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Mistakes in mouse models of IBD and how to avoid them

Anje te Velde, Pim J Koelink

Summary

AI Generated

Experimental colitis models used to study IBD pathophysiology and develop treatments have limited predictive value for clinical therapeutic targets despite more than 50 available models.

  • More than 50 experimental colitis models exist but have limited use in predicting the clinical relevance of therapeutic targets in IBD
  • The models broadly fit into groups including spontaneous colitis, induced colitis from genetic abnormality, induced colitis from targeted mutation or transgene introduction, induced colitis from exogenous causative agents, and induction by immune system manipulation
  • There is a necessity to improve the methodological quality of animal studies in this field
Download PDF

Was this helpful?

Thanks for your feedback.

This summary was generated by an AI large language model based on the content transcript. It is for informational purposes only and should not be considered a substitute for clinical judgment. Always rely on your professional expertise and the full clinical context when making clinical decisions.

References

Mistakes
References
Mistake 1 Mistake 2 Mistake 3 Mistake 4 Mistake 5 Mistake 6 Mistake 7 Mistake 8 Mistake 9 Mistake 10
1.
Bouma G and Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol 2003; 3: 521–533.  [Link]
2.
Khanna PV, et al. Use of animal models in elucidating disease pathogenesis in IBD. Semin Immunopathol 2014; 36: 541–551.  [Link]
3.
Mizoguchi A and Mizoguchi E. Animal models of IBD: linkage to human disease. Curr Opin Pharmacol 2010; 10: 578–587.  [Link]
4.
Uhlig HH and Powrie F. Mouse models of intestinal inflammation as tools to understand the pathogenesis of inflammatory bowel disease. Eur J Immunol 2009; 39: 2021–2026.  [Link]
5.
Zeeff SB, Kunne C, Bouma G, et al. Actual usage and quality of experimental colitis models in preclinical efficacy testing: a scoping review. Inflamm Bowel Dis Prepublished April 21, 20016, DOI: 10.1097/MIB.0000000000000758.  [Link]
6.
DeVoss J and Diehl L. Murine models of inflammatory bowel disease (IBD): challenges of modeling human disease. Toxicol Pathol 2014; 42: 99–110.  [Link]
7.
Goyal N, et al. Animal models of inflammatory bowel disease: a review. Inflammopharmacology 2014; 22: 219–33. [Link]
8.
Jones-Hall YL and Grisham MB. Immunopathological characterization of selected mouse models of inflammatory bowel disease: Comparison to human disease. Pathophysiology 2014; 21: 267–88.  [Link]
9.
te Velde AA, et al. Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease. Inflamm Bowel Dis 2007; 13: 325–330.  [Link]
10.
te Velde AA, Verstege MI and Hommes DW. Critical appraisal of the current practice in murine TNBS-induced colitis. Inflamm Bowel Dis 2006; 12: 995–999.  [Link]
11.
Wirtz S, et al. Chemically induced mouse models of intestinal inflammation. Nat Protoc 2007; 2: 541–546.  [Link]
12.
Read S and Powrie F. Induction of inflammatory bowel disease in immunodeficient mice by depletion of regulatory T cells. Curr Protoc Immunol 1999; 30 (suppl): 15.13.1–15.13.10.  [Link]
13.
Ostanin DV, et al. T cell transfer model of chronic colitis: concepts, considerations, and tricks of the trade. Am J Physiol Gastrointest Liver Physiol 2009; 296: G135–G146.  [Link]
14.
National Academies of Sciences, Engineering, and Medicine. Reproducibility Issues in Research with Animals and Animal Models: Workshop in Brief. Washington, DC: The National Academies Press, 2015.
15.
Prinz F, Schlange T and Asadullah K. Believe it or not: how much can we rely on published data on potential drug targets? Nat Rev Drug Discov 2011; 10: 712.  [Link]
16.
Nature. Chow down. Nature 2016; 530: 254.  [Link]
17.
Reardon S. A mouse's house may ruin experiments. Nature 2016; 530: 264.  [Link]
18.
Gkouskou KK, et al. The gut microbiota in mouse models of inflammatory bowel disease. Front Cell Infect Microbiol 2014; 4: 28.  [Link]
19.
Macpherson AJ and McCoy KD. Standardised animal models of host microbial mutualism. Mucosal Immunol 2015; 8: 476–486.  [Link]
20.
Hooijmans CR, et al. SYRCLE's risk of bias tool for animal studies. BMC Med Res Methodol 2014; 14: 43.  [Link]
21.
Erben U, et al. A guide to histomorphological evaluation of intestinal inflammation in mouse models. Int J Clin Exp Pathol 2014; 7: 4557–4576.  [Link]
22.
Gibson-Corley KN, Olivier AK and Meyerholz DK.  Principles for valid histopathologic scoring in research. Vet Pathol 2013; 50: 1007–1015.  [Link]
23.
Hansen AK, et al. Impact of the gut microbiota on rodent models of human disease. World J Gastroenterol 2014; 20: 17727–17736.  [Link]
24.
Schoeb TR and Bullard DC. Microbial and histopathologic considerations in the use of mouse models of inflammatory bowel diseases. Inflamm Bowel Dis 2012; 18: 1558–1565.  [Link]
25.
Hansen AK, et al. A review of applied aspects of dealing with gut microbiota impact on rodent models. ILAR J, 2015; 56: 250–264.  [Link]
26.
Jakobsson HE, et al. The composition of the gut microbiota shapes the colon mucus barrier. EMBO Rep 2015; 16: 164–177.  [Link]
27.
Ivanov II, et al. Induction of intestinal Th17 cells by segmented filamentous bacteria. Cell 2009; 139: 485–498.  [Link]
28.
Ericsson AC, et al. Effects of vendor and genetic background on the composition of the fecal microbiota of inbred mice. PLoS One 2015: 10: e0116704.  [Link]
29.
Zenewicz LA, et al. IL-22 deficiency alters colonoc microbiota to be transmissable and colitogenic. J Immunol 2013; 190: 5306–5312.  [Link]
30.
Mahler M, et al. Differential susceptibility of inbred mouse strains to dextran sulfate sodium-induced colitis. Am J Physiol 1998; 274: G544–G551.  [Link]
31.
Melgar S, Karlsson A and Michaelsson E. Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation. Am J Physiol Gastrointest Liver Physiol 2005; 288: G1328–G1338.  [Link]
32.
Scheiffele F and Fuss IJ. Induction of TNBS colitis in mice. Curr Protoc Immunol 2002; Chapter 15: Unit 15.19.  [Link]
33.
Bouma G, Kaushiva A and Strober W. Experimental murine colitis is regulated by two genetic loci, including one on chromosome 11 that regulates IL-12 responses. Gastroenterology 2002; 123: 554–565.  [Link]
34.
Hsieh CS, et al. T cell genetic background determines default T helper phenotype development in vitro. J Exp Med 1995; 181: 713–721.  [Link]
35.
Powrie F, et al. Inhibition of Th1 responses prevents inflammatory bowel disease in scid mice reconstituted with CD45RBhi CD4+ T cells. Immunity 1994; 1: 553–562.  [Link]
36.
Berg DJ, et al. Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses. J Clin Invest 1996; 98: 1010–1020.  [Link]
37.
Beckwith J, et al. Cdcs1, a major colitogenic locus in mice, regulates innate and adaptive immune response to enteric bacterial antigens. Gastroenterology 2005; 129: 1473–1484.  [Link]
38.
Holgersen K, et al. Characterisation of enterocolitis in the piroxicam-accelerated interleukin-10 knock out mouse—a model mimicking inflammatory bowel disease. J Crohns Colitis 2014; 8: 147–160.  [Link]
39.
Atamni HJ, et al. High-fat-diet induced development of increased fasting glucose levels and impaired response to intraperitoneal glucose challenge in the collaborative cross mouse genetic reference population. BMC Genet 2016; 17: 10.  [Link]
40.
Aylor DL, et al. Genetic analysis of complex traits in the emerging Collaborative Cross. Genome Res 2011; 21:  1213–1222.  [Link]
41.
Ngo ST, Steyn FJ and McCombe PA. Gender differences in autoimmune disease. Front Neuroendocrinol 2014; 35: 347–369.  [Link]
42.
Babickova J, et al. Sex differences in experimentally induced colitis in mice: a role for estrogens. Inflammation 2015; 38: 1996–2006.  [Link]
43.
te Velde AA, et al. Effects of dietary plant sterols and stanol esters with low- and high-fat diets in chronic and acute models for experimental colitis. Nutrients 2015; 7: 8518–8531.  [Link]
44.
Berglund M, et al. Gender dependent importance of IRAK-1 in dextran sulfate sodium induced colitis. Cell Immunol 2009; 259: 27–32.  [Link]
45.
Alex P, et al. Distinct cytokine patterns identified from multiplex profiles of murine DSS and TNBS-induced colitis. Inflamm Bowel Dis 2009; 15: 341–352.  [Link]
46.
Gonder JC and Laber K. A renewed look at laboratory rodent housing and management. ILAR J 2007; 48: 29–36.  [Link]
47.
Bramhall M, et al. Quality of methods reporting in animal models of colitis. Inflamm Bowel Dis 2015; 21: 1248–1259.  [Link]
48.
Kilkenny C, et al. Improving bioscience research reporting: the ARRIVE guidelines for reporting animal research. PLoS Biol 2010; 8: e1000412.  [Link]
49.
Koboziev I, et al. Pharmacological intervention studies using mouse models of the inflammatory bowel diseases: translating preclinical data into new drug therapies. Inflamm Bowel Dis 2011; 17: 1229–1245.  [Link]
50.
Koelink PJ, Wildenberg ME, Stitt LW, Feagan BG, Koldijk M, Van ‘T Wout AB, et al. Development of Reliable, Valid and Responsive Scoring Systems for Endoscopy and Histology in Animal Models for Inflammatory Bowel Disease. Journal of Crohn’s and Colitis. 2018 Jun 28;12(7):794–803.
51.
[url:https://academic.oup.com/ecco-jcc/article/12/7/794/4955731?login=false]
52.
Valatas V, Vakas M and Kolios G. The value of experimental models of colitis in predicting efficacy of biological therapies for inflammatory bowel diseases. Am J Physiol Gastrointest Liver Physiol 2013; 305: G763–G785.  [Link]
53.
Prattis S and Jurjus A. Spontaneous and transgenic rodent models of inflammatory bowel disease. Lab Anim Res 2015; 31: 47–68.  [Link]

Abstract

Experimental colitis models are used to study the pathophysiology of inflammatory bowel disease (IBD) and develop new treatments. There are more than 50 models, but they have limited use in predicting the clinical relevance of therapeutic targets in IBD. These models broadly fit into four groups: spontaneous colitis, induced colitis from genetic abnormality, induced colitis from targeted mutation or transgene introduction, induced colitis from exogenous causative agents, and induction of colitis by manipulation of the immune system. There is a necessity to improve the methodological quality of animal studies.

Topics

IBD

Citation

 Koelink PJ and te Velde AA. Mistakes in mouse models of IBD and how to avoid them. UEG Education 2016: 16: 11–14.

Published

2024

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UEG Mistakes In Articles
Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

Log in to continue.

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Log In Create a free account

Not sure what you can access? Learn more about account types.

Mistakes in transitional care for children and young adults and how to avoid them

Patrizia Burra, Hans Törnblom, Jorge Amil Dias, Moriam Mustapha

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

This summary was generated by an AI large language model based on the content transcript. It is for informational purposes only and should not be considered a substitute for clinical judgment. Always rely on your professional expertise and the full clinical context when making clinical decisions.

References

Mistakes
References
Mistake 1 Mistake 2 Mistake 3 Mistake 4 Mistake 5 Mistake 6 Mistake 7 Mistake 8 Mistake 9 Mistake 10
1.
Bouma G and Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol 2003; 3: 521–533.  [Link]
2.
Khanna PV, et al. Use of animal models in elucidating disease pathogenesis in IBD. Semin Immunopathol 2014; 36: 541–551.  [Link]
3.
Mizoguchi A and Mizoguchi E. Animal models of IBD: linkage to human disease. Curr Opin Pharmacol 2010; 10: 578–587.  [Link]
4.
Uhlig HH and Powrie F. Mouse models of intestinal inflammation as tools to understand the pathogenesis of inflammatory bowel disease. Eur J Immunol 2009; 39: 2021–2026.  [Link]
5.
Zeeff SB, Kunne C, Bouma G, et al. Actual usage and quality of experimental colitis models in preclinical efficacy testing: a scoping review. Inflamm Bowel Dis Prepublished April 21, 20016, DOI: 10.1097/MIB.0000000000000758.  [Link]
6.
DeVoss J and Diehl L. Murine models of inflammatory bowel disease (IBD): challenges of modeling human disease. Toxicol Pathol 2014; 42: 99–110.  [Link]
7.
Goyal N, et al. Animal models of inflammatory bowel disease: a review. Inflammopharmacology 2014; 22: 219–33. [Link]
8.
Jones-Hall YL and Grisham MB. Immunopathological characterization of selected mouse models of inflammatory bowel disease: Comparison to human disease. Pathophysiology 2014; 21: 267–88.  [Link]
9.
te Velde AA, et al. Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease. Inflamm Bowel Dis 2007; 13: 325–330.  [Link]
10.
te Velde AA, Verstege MI and Hommes DW. Critical appraisal of the current practice in murine TNBS-induced colitis. Inflamm Bowel Dis 2006; 12: 995–999.  [Link]
11.
Wirtz S, et al. Chemically induced mouse models of intestinal inflammation. Nat Protoc 2007; 2: 541–546.  [Link]
12.
Read S and Powrie F. Induction of inflammatory bowel disease in immunodeficient mice by depletion of regulatory T cells. Curr Protoc Immunol 1999; 30 (suppl): 15.13.1–15.13.10.  [Link]
13.
Ostanin DV, et al. T cell transfer model of chronic colitis: concepts, considerations, and tricks of the trade. Am J Physiol Gastrointest Liver Physiol 2009; 296: G135–G146.  [Link]
14.
National Academies of Sciences, Engineering, and Medicine. Reproducibility Issues in Research with Animals and Animal Models: Workshop in Brief. Washington, DC: The National Academies Press, 2015.
15.
Prinz F, Schlange T and Asadullah K. Believe it or not: how much can we rely on published data on potential drug targets? Nat Rev Drug Discov 2011; 10: 712.  [Link]
16.
Nature. Chow down. Nature 2016; 530: 254.  [Link]
17.
Reardon S. A mouse's house may ruin experiments. Nature 2016; 530: 264.  [Link]
18.
Gkouskou KK, et al. The gut microbiota in mouse models of inflammatory bowel disease. Front Cell Infect Microbiol 2014; 4: 28.  [Link]
19.
Macpherson AJ and McCoy KD. Standardised animal models of host microbial mutualism. Mucosal Immunol 2015; 8: 476–486.  [Link]
20.
Hooijmans CR, et al. SYRCLE's risk of bias tool for animal studies. BMC Med Res Methodol 2014; 14: 43.  [Link]
21.
Erben U, et al. A guide to histomorphological evaluation of intestinal inflammation in mouse models. Int J Clin Exp Pathol 2014; 7: 4557–4576.  [Link]
22.
Gibson-Corley KN, Olivier AK and Meyerholz DK.  Principles for valid histopathologic scoring in research. Vet Pathol 2013; 50: 1007–1015.  [Link]
23.
Hansen AK, et al. Impact of the gut microbiota on rodent models of human disease. World J Gastroenterol 2014; 20: 17727–17736.  [Link]
24.
Schoeb TR and Bullard DC. Microbial and histopathologic considerations in the use of mouse models of inflammatory bowel diseases. Inflamm Bowel Dis 2012; 18: 1558–1565.  [Link]
25.
Hansen AK, et al. A review of applied aspects of dealing with gut microbiota impact on rodent models. ILAR J, 2015; 56: 250–264.  [Link]
26.
Jakobsson HE, et al. The composition of the gut microbiota shapes the colon mucus barrier. EMBO Rep 2015; 16: 164–177.  [Link]
27.
Ivanov II, et al. Induction of intestinal Th17 cells by segmented filamentous bacteria. Cell 2009; 139: 485–498.  [Link]
28.
Ericsson AC, et al. Effects of vendor and genetic background on the composition of the fecal microbiota of inbred mice. PLoS One 2015: 10: e0116704.  [Link]
29.
Zenewicz LA, et al. IL-22 deficiency alters colonoc microbiota to be transmissable and colitogenic. J Immunol 2013; 190: 5306–5312.  [Link]
30.
Mahler M, et al. Differential susceptibility of inbred mouse strains to dextran sulfate sodium-induced colitis. Am J Physiol 1998; 274: G544–G551.  [Link]
31.
Melgar S, Karlsson A and Michaelsson E. Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation. Am J Physiol Gastrointest Liver Physiol 2005; 288: G1328–G1338.  [Link]
32.
Scheiffele F and Fuss IJ. Induction of TNBS colitis in mice. Curr Protoc Immunol 2002; Chapter 15: Unit 15.19.  [Link]
33.
Bouma G, Kaushiva A and Strober W. Experimental murine colitis is regulated by two genetic loci, including one on chromosome 11 that regulates IL-12 responses. Gastroenterology 2002; 123: 554–565.  [Link]
34.
Hsieh CS, et al. T cell genetic background determines default T helper phenotype development in vitro. J Exp Med 1995; 181: 713–721.  [Link]
35.
Powrie F, et al. Inhibition of Th1 responses prevents inflammatory bowel disease in scid mice reconstituted with CD45RBhi CD4+ T cells. Immunity 1994; 1: 553–562.  [Link]
36.
Berg DJ, et al. Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses. J Clin Invest 1996; 98: 1010–1020.  [Link]
37.
Beckwith J, et al. Cdcs1, a major colitogenic locus in mice, regulates innate and adaptive immune response to enteric bacterial antigens. Gastroenterology 2005; 129: 1473–1484.  [Link]
38.
Holgersen K, et al. Characterisation of enterocolitis in the piroxicam-accelerated interleukin-10 knock out mouse—a model mimicking inflammatory bowel disease. J Crohns Colitis 2014; 8: 147–160.  [Link]
39.
Atamni HJ, et al. High-fat-diet induced development of increased fasting glucose levels and impaired response to intraperitoneal glucose challenge in the collaborative cross mouse genetic reference population. BMC Genet 2016; 17: 10.  [Link]
40.
Aylor DL, et al. Genetic analysis of complex traits in the emerging Collaborative Cross. Genome Res 2011; 21:  1213–1222.  [Link]
41.
Ngo ST, Steyn FJ and McCombe PA. Gender differences in autoimmune disease. Front Neuroendocrinol 2014; 35: 347–369.  [Link]
42.
Babickova J, et al. Sex differences in experimentally induced colitis in mice: a role for estrogens. Inflammation 2015; 38: 1996–2006.  [Link]
43.
te Velde AA, et al. Effects of dietary plant sterols and stanol esters with low- and high-fat diets in chronic and acute models for experimental colitis. Nutrients 2015; 7: 8518–8531.  [Link]
44.
Berglund M, et al. Gender dependent importance of IRAK-1 in dextran sulfate sodium induced colitis. Cell Immunol 2009; 259: 27–32.  [Link]
45.
Alex P, et al. Distinct cytokine patterns identified from multiplex profiles of murine DSS and TNBS-induced colitis. Inflamm Bowel Dis 2009; 15: 341–352.  [Link]
46.
Gonder JC and Laber K. A renewed look at laboratory rodent housing and management. ILAR J 2007; 48: 29–36.  [Link]
47.
Bramhall M, et al. Quality of methods reporting in animal models of colitis. Inflamm Bowel Dis 2015; 21: 1248–1259.  [Link]
48.
Kilkenny C, et al. Improving bioscience research reporting: the ARRIVE guidelines for reporting animal research. PLoS Biol 2010; 8: e1000412.  [Link]
49.
Koboziev I, et al. Pharmacological intervention studies using mouse models of the inflammatory bowel diseases: translating preclinical data into new drug therapies. Inflamm Bowel Dis 2011; 17: 1229–1245.  [Link]
50.
Koelink PJ, Wildenberg ME, Stitt LW, Feagan BG, Koldijk M, Van ‘T Wout AB, et al. Development of Reliable, Valid and Responsive Scoring Systems for Endoscopy and Histology in Animal Models for Inflammatory Bowel Disease. Journal of Crohn’s and Colitis. 2018 Jun 28;12(7):794–803.
51.
[url:https://academic.oup.com/ecco-jcc/article/12/7/794/4955731?login=false]
52.
Valatas V, Vakas M and Kolios G. The value of experimental models of colitis in predicting efficacy of biological therapies for inflammatory bowel diseases. Am J Physiol Gastrointest Liver Physiol 2013; 305: G763–G785.  [Link]
53.
Prattis S and Jurjus A. Spontaneous and transgenic rodent models of inflammatory bowel disease. Lab Anim Res 2015; 31: 47–68.  [Link]

Abstract

Children and adolescents with chronic diseases requiring lifelong care face unique challenges that affect their daily lives and those of their families. Initially, these patients receive specialized care in pediatric facilities, where parents play a key role in treatment decisions. However, transitioning to adult healthcare facilities is inevitable, and this process, recognized as crucial years ago, involves moving adolescents with chronic conditions from child-centered to adult-oriented care. This transition can be complicated by varying age limits for pediatric care and the scarcity of adult care centers with specific expertise. The transition often requires cooperation between different centers or even countries due to patient mobility. The transition phase is critical, as it can lead to loss of follow-up, treatment suspension, and increased risks of complications or disease relapse. Beyond medical management, various factors influence the long-term prognosis of chronic conditions, making a well-organized transition program essential. While many hospitals have implemented transition models with mixed results in satisfaction, disease control, and follow-up adherence, there are frequent shortcomings in the process. This Mistakes In article will outline eight common mistakes made during the transition from pediatric to adult care, supported by literature and professional experience.

Topics

Primary Care

Citation

Jorge Amil-Dias, Hans Törnblom, Moriam Mustapha and Patrizia Burra. Mistakes in transitional care for children and young adults and how to avoid them. UEG Education 2023; 23: 22-25.

Published

2023

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UEG Mistakes In Articles
Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

Log in to continue.

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Log In Create a free account

Not sure what you can access? Learn more about account types.

Mistakes in short bowel and how to avoid them

Simon Gabe, Jeremy Nightingale, Siddhartha Oke

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

This summary was generated by an AI large language model based on the content transcript. It is for informational purposes only and should not be considered a substitute for clinical judgment. Always rely on your professional expertise and the full clinical context when making clinical decisions.

References

Mistakes
References
Mistake 1 Mistake 2 Mistake 3 Mistake 4 Mistake 5 Mistake 6 Mistake 7 Mistake 8 Mistake 9 Mistake 10
1.
Bouma G and Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol 2003; 3: 521–533.  [Link]
2.
Khanna PV, et al. Use of animal models in elucidating disease pathogenesis in IBD. Semin Immunopathol 2014; 36: 541–551.  [Link]
3.
Mizoguchi A and Mizoguchi E. Animal models of IBD: linkage to human disease. Curr Opin Pharmacol 2010; 10: 578–587.  [Link]
4.
Uhlig HH and Powrie F. Mouse models of intestinal inflammation as tools to understand the pathogenesis of inflammatory bowel disease. Eur J Immunol 2009; 39: 2021–2026.  [Link]
5.
Zeeff SB, Kunne C, Bouma G, et al. Actual usage and quality of experimental colitis models in preclinical efficacy testing: a scoping review. Inflamm Bowel Dis Prepublished April 21, 20016, DOI: 10.1097/MIB.0000000000000758.  [Link]
6.
DeVoss J and Diehl L. Murine models of inflammatory bowel disease (IBD): challenges of modeling human disease. Toxicol Pathol 2014; 42: 99–110.  [Link]
7.
Goyal N, et al. Animal models of inflammatory bowel disease: a review. Inflammopharmacology 2014; 22: 219–33. [Link]
8.
Jones-Hall YL and Grisham MB. Immunopathological characterization of selected mouse models of inflammatory bowel disease: Comparison to human disease. Pathophysiology 2014; 21: 267–88.  [Link]
9.
te Velde AA, et al. Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease. Inflamm Bowel Dis 2007; 13: 325–330.  [Link]
10.
te Velde AA, Verstege MI and Hommes DW. Critical appraisal of the current practice in murine TNBS-induced colitis. Inflamm Bowel Dis 2006; 12: 995–999.  [Link]
11.
Wirtz S, et al. Chemically induced mouse models of intestinal inflammation. Nat Protoc 2007; 2: 541–546.  [Link]
12.
Read S and Powrie F. Induction of inflammatory bowel disease in immunodeficient mice by depletion of regulatory T cells. Curr Protoc Immunol 1999; 30 (suppl): 15.13.1–15.13.10.  [Link]
13.
Ostanin DV, et al. T cell transfer model of chronic colitis: concepts, considerations, and tricks of the trade. Am J Physiol Gastrointest Liver Physiol 2009; 296: G135–G146.  [Link]
14.
National Academies of Sciences, Engineering, and Medicine. Reproducibility Issues in Research with Animals and Animal Models: Workshop in Brief. Washington, DC: The National Academies Press, 2015.
15.
Prinz F, Schlange T and Asadullah K. Believe it or not: how much can we rely on published data on potential drug targets? Nat Rev Drug Discov 2011; 10: 712.  [Link]
16.
Nature. Chow down. Nature 2016; 530: 254.  [Link]
17.
Reardon S. A mouse's house may ruin experiments. Nature 2016; 530: 264.  [Link]
18.
Gkouskou KK, et al. The gut microbiota in mouse models of inflammatory bowel disease. Front Cell Infect Microbiol 2014; 4: 28.  [Link]
19.
Macpherson AJ and McCoy KD. Standardised animal models of host microbial mutualism. Mucosal Immunol 2015; 8: 476–486.  [Link]
20.
Hooijmans CR, et al. SYRCLE's risk of bias tool for animal studies. BMC Med Res Methodol 2014; 14: 43.  [Link]
21.
Erben U, et al. A guide to histomorphological evaluation of intestinal inflammation in mouse models. Int J Clin Exp Pathol 2014; 7: 4557–4576.  [Link]
22.
Gibson-Corley KN, Olivier AK and Meyerholz DK.  Principles for valid histopathologic scoring in research. Vet Pathol 2013; 50: 1007–1015.  [Link]
23.
Hansen AK, et al. Impact of the gut microbiota on rodent models of human disease. World J Gastroenterol 2014; 20: 17727–17736.  [Link]
24.
Schoeb TR and Bullard DC. Microbial and histopathologic considerations in the use of mouse models of inflammatory bowel diseases. Inflamm Bowel Dis 2012; 18: 1558–1565.  [Link]
25.
Hansen AK, et al. A review of applied aspects of dealing with gut microbiota impact on rodent models. ILAR J, 2015; 56: 250–264.  [Link]
26.
Jakobsson HE, et al. The composition of the gut microbiota shapes the colon mucus barrier. EMBO Rep 2015; 16: 164–177.  [Link]
27.
Ivanov II, et al. Induction of intestinal Th17 cells by segmented filamentous bacteria. Cell 2009; 139: 485–498.  [Link]
28.
Ericsson AC, et al. Effects of vendor and genetic background on the composition of the fecal microbiota of inbred mice. PLoS One 2015: 10: e0116704.  [Link]
29.
Zenewicz LA, et al. IL-22 deficiency alters colonoc microbiota to be transmissable and colitogenic. J Immunol 2013; 190: 5306–5312.  [Link]
30.
Mahler M, et al. Differential susceptibility of inbred mouse strains to dextran sulfate sodium-induced colitis. Am J Physiol 1998; 274: G544–G551.  [Link]
31.
Melgar S, Karlsson A and Michaelsson E. Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation. Am J Physiol Gastrointest Liver Physiol 2005; 288: G1328–G1338.  [Link]
32.
Scheiffele F and Fuss IJ. Induction of TNBS colitis in mice. Curr Protoc Immunol 2002; Chapter 15: Unit 15.19.  [Link]
33.
Bouma G, Kaushiva A and Strober W. Experimental murine colitis is regulated by two genetic loci, including one on chromosome 11 that regulates IL-12 responses. Gastroenterology 2002; 123: 554–565.  [Link]
34.
Hsieh CS, et al. T cell genetic background determines default T helper phenotype development in vitro. J Exp Med 1995; 181: 713–721.  [Link]
35.
Powrie F, et al. Inhibition of Th1 responses prevents inflammatory bowel disease in scid mice reconstituted with CD45RBhi CD4+ T cells. Immunity 1994; 1: 553–562.  [Link]
36.
Berg DJ, et al. Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses. J Clin Invest 1996; 98: 1010–1020.  [Link]
37.
Beckwith J, et al. Cdcs1, a major colitogenic locus in mice, regulates innate and adaptive immune response to enteric bacterial antigens. Gastroenterology 2005; 129: 1473–1484.  [Link]
38.
Holgersen K, et al. Characterisation of enterocolitis in the piroxicam-accelerated interleukin-10 knock out mouse—a model mimicking inflammatory bowel disease. J Crohns Colitis 2014; 8: 147–160.  [Link]
39.
Atamni HJ, et al. High-fat-diet induced development of increased fasting glucose levels and impaired response to intraperitoneal glucose challenge in the collaborative cross mouse genetic reference population. BMC Genet 2016; 17: 10.  [Link]
40.
Aylor DL, et al. Genetic analysis of complex traits in the emerging Collaborative Cross. Genome Res 2011; 21:  1213–1222.  [Link]
41.
Ngo ST, Steyn FJ and McCombe PA. Gender differences in autoimmune disease. Front Neuroendocrinol 2014; 35: 347–369.  [Link]
42.
Babickova J, et al. Sex differences in experimentally induced colitis in mice: a role for estrogens. Inflammation 2015; 38: 1996–2006.  [Link]
43.
te Velde AA, et al. Effects of dietary plant sterols and stanol esters with low- and high-fat diets in chronic and acute models for experimental colitis. Nutrients 2015; 7: 8518–8531.  [Link]
44.
Berglund M, et al. Gender dependent importance of IRAK-1 in dextran sulfate sodium induced colitis. Cell Immunol 2009; 259: 27–32.  [Link]
45.
Alex P, et al. Distinct cytokine patterns identified from multiplex profiles of murine DSS and TNBS-induced colitis. Inflamm Bowel Dis 2009; 15: 341–352.  [Link]
46.
Gonder JC and Laber K. A renewed look at laboratory rodent housing and management. ILAR J 2007; 48: 29–36.  [Link]
47.
Bramhall M, et al. Quality of methods reporting in animal models of colitis. Inflamm Bowel Dis 2015; 21: 1248–1259.  [Link]
48.
Kilkenny C, et al. Improving bioscience research reporting: the ARRIVE guidelines for reporting animal research. PLoS Biol 2010; 8: e1000412.  [Link]
49.
Koboziev I, et al. Pharmacological intervention studies using mouse models of the inflammatory bowel diseases: translating preclinical data into new drug therapies. Inflamm Bowel Dis 2011; 17: 1229–1245.  [Link]
50.
Koelink PJ, Wildenberg ME, Stitt LW, Feagan BG, Koldijk M, Van ‘T Wout AB, et al. Development of Reliable, Valid and Responsive Scoring Systems for Endoscopy and Histology in Animal Models for Inflammatory Bowel Disease. Journal of Crohn’s and Colitis. 2018 Jun 28;12(7):794–803.
51.
[url:https://academic.oup.com/ecco-jcc/article/12/7/794/4955731?login=false]
52.
Valatas V, Vakas M and Kolios G. The value of experimental models of colitis in predicting efficacy of biological therapies for inflammatory bowel diseases. Am J Physiol Gastrointest Liver Physiol 2013; 305: G763–G785.  [Link]
53.
Prattis S and Jurjus A. Spontaneous and transgenic rodent models of inflammatory bowel disease. Lab Anim Res 2015; 31: 47–68.  [Link]

Abstract

Short bowel is a condition that occurs after single or multiple intestinal resections. The incidence of short bowel in Europe is 2 per million of the population and it carries with it lifelong morbidity and mortality. The initial recognition and management of short bowel in the adult population tends to occur in the postoperative period and in the secondary care setting, where specialist input from clinicians experienced in short bowel is often lacking.

Topics

Small Intestine & Nutrition

Citation

Oke SM, Nightingale JM and Gabe SM Mistakes in short bowel and how to avoid them. UEG Education 2018; 18: 7–11.

Published

2018

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UEG Mistakes In Articles
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Mistakes in bariatric surgery and how to avoid them

Francesco Saverio Papadia, Gianni Camerini

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Summary is not available for this content yet.

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This summary was generated by an AI large language model based on the content transcript. It is for informational purposes only and should not be considered a substitute for clinical judgment. Always rely on your professional expertise and the full clinical context when making clinical decisions.

References

Mistakes
References
Mistake 1 Mistake 2 Mistake 3 Mistake 4 Mistake 5 Mistake 6 Mistake 7 Mistake 8 Mistake 9 Mistake 10
1.
Bouma G and Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol 2003; 3: 521–533.  [Link]
2.
Khanna PV, et al. Use of animal models in elucidating disease pathogenesis in IBD. Semin Immunopathol 2014; 36: 541–551.  [Link]
3.
Mizoguchi A and Mizoguchi E. Animal models of IBD: linkage to human disease. Curr Opin Pharmacol 2010; 10: 578–587.  [Link]
4.
Uhlig HH and Powrie F. Mouse models of intestinal inflammation as tools to understand the pathogenesis of inflammatory bowel disease. Eur J Immunol 2009; 39: 2021–2026.  [Link]
5.
Zeeff SB, Kunne C, Bouma G, et al. Actual usage and quality of experimental colitis models in preclinical efficacy testing: a scoping review. Inflamm Bowel Dis Prepublished April 21, 20016, DOI: 10.1097/MIB.0000000000000758.  [Link]
6.
DeVoss J and Diehl L. Murine models of inflammatory bowel disease (IBD): challenges of modeling human disease. Toxicol Pathol 2014; 42: 99–110.  [Link]
7.
Goyal N, et al. Animal models of inflammatory bowel disease: a review. Inflammopharmacology 2014; 22: 219–33. [Link]
8.
Jones-Hall YL and Grisham MB. Immunopathological characterization of selected mouse models of inflammatory bowel disease: Comparison to human disease. Pathophysiology 2014; 21: 267–88.  [Link]
9.
te Velde AA, et al. Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease. Inflamm Bowel Dis 2007; 13: 325–330.  [Link]
10.
te Velde AA, Verstege MI and Hommes DW. Critical appraisal of the current practice in murine TNBS-induced colitis. Inflamm Bowel Dis 2006; 12: 995–999.  [Link]
11.
Wirtz S, et al. Chemically induced mouse models of intestinal inflammation. Nat Protoc 2007; 2: 541–546.  [Link]
12.
Read S and Powrie F. Induction of inflammatory bowel disease in immunodeficient mice by depletion of regulatory T cells. Curr Protoc Immunol 1999; 30 (suppl): 15.13.1–15.13.10.  [Link]
13.
Ostanin DV, et al. T cell transfer model of chronic colitis: concepts, considerations, and tricks of the trade. Am J Physiol Gastrointest Liver Physiol 2009; 296: G135–G146.  [Link]
14.
National Academies of Sciences, Engineering, and Medicine. Reproducibility Issues in Research with Animals and Animal Models: Workshop in Brief. Washington, DC: The National Academies Press, 2015.
15.
Prinz F, Schlange T and Asadullah K. Believe it or not: how much can we rely on published data on potential drug targets? Nat Rev Drug Discov 2011; 10: 712.  [Link]
16.
Nature. Chow down. Nature 2016; 530: 254.  [Link]
17.
Reardon S. A mouse's house may ruin experiments. Nature 2016; 530: 264.  [Link]
18.
Gkouskou KK, et al. The gut microbiota in mouse models of inflammatory bowel disease. Front Cell Infect Microbiol 2014; 4: 28.  [Link]
19.
Macpherson AJ and McCoy KD. Standardised animal models of host microbial mutualism. Mucosal Immunol 2015; 8: 476–486.  [Link]
20.
Hooijmans CR, et al. SYRCLE's risk of bias tool for animal studies. BMC Med Res Methodol 2014; 14: 43.  [Link]
21.
Erben U, et al. A guide to histomorphological evaluation of intestinal inflammation in mouse models. Int J Clin Exp Pathol 2014; 7: 4557–4576.  [Link]
22.
Gibson-Corley KN, Olivier AK and Meyerholz DK.  Principles for valid histopathologic scoring in research. Vet Pathol 2013; 50: 1007–1015.  [Link]
23.
Hansen AK, et al. Impact of the gut microbiota on rodent models of human disease. World J Gastroenterol 2014; 20: 17727–17736.  [Link]
24.
Schoeb TR and Bullard DC. Microbial and histopathologic considerations in the use of mouse models of inflammatory bowel diseases. Inflamm Bowel Dis 2012; 18: 1558–1565.  [Link]
25.
Hansen AK, et al. A review of applied aspects of dealing with gut microbiota impact on rodent models. ILAR J, 2015; 56: 250–264.  [Link]
26.
Jakobsson HE, et al. The composition of the gut microbiota shapes the colon mucus barrier. EMBO Rep 2015; 16: 164–177.  [Link]
27.
Ivanov II, et al. Induction of intestinal Th17 cells by segmented filamentous bacteria. Cell 2009; 139: 485–498.  [Link]
28.
Ericsson AC, et al. Effects of vendor and genetic background on the composition of the fecal microbiota of inbred mice. PLoS One 2015: 10: e0116704.  [Link]
29.
Zenewicz LA, et al. IL-22 deficiency alters colonoc microbiota to be transmissable and colitogenic. J Immunol 2013; 190: 5306–5312.  [Link]
30.
Mahler M, et al. Differential susceptibility of inbred mouse strains to dextran sulfate sodium-induced colitis. Am J Physiol 1998; 274: G544–G551.  [Link]
31.
Melgar S, Karlsson A and Michaelsson E. Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation. Am J Physiol Gastrointest Liver Physiol 2005; 288: G1328–G1338.  [Link]
32.
Scheiffele F and Fuss IJ. Induction of TNBS colitis in mice. Curr Protoc Immunol 2002; Chapter 15: Unit 15.19.  [Link]
33.
Bouma G, Kaushiva A and Strober W. Experimental murine colitis is regulated by two genetic loci, including one on chromosome 11 that regulates IL-12 responses. Gastroenterology 2002; 123: 554–565.  [Link]
34.
Hsieh CS, et al. T cell genetic background determines default T helper phenotype development in vitro. J Exp Med 1995; 181: 713–721.  [Link]
35.
Powrie F, et al. Inhibition of Th1 responses prevents inflammatory bowel disease in scid mice reconstituted with CD45RBhi CD4+ T cells. Immunity 1994; 1: 553–562.  [Link]
36.
Berg DJ, et al. Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses. J Clin Invest 1996; 98: 1010–1020.  [Link]
37.
Beckwith J, et al. Cdcs1, a major colitogenic locus in mice, regulates innate and adaptive immune response to enteric bacterial antigens. Gastroenterology 2005; 129: 1473–1484.  [Link]
38.
Holgersen K, et al. Characterisation of enterocolitis in the piroxicam-accelerated interleukin-10 knock out mouse—a model mimicking inflammatory bowel disease. J Crohns Colitis 2014; 8: 147–160.  [Link]
39.
Atamni HJ, et al. High-fat-diet induced development of increased fasting glucose levels and impaired response to intraperitoneal glucose challenge in the collaborative cross mouse genetic reference population. BMC Genet 2016; 17: 10.  [Link]
40.
Aylor DL, et al. Genetic analysis of complex traits in the emerging Collaborative Cross. Genome Res 2011; 21:  1213–1222.  [Link]
41.
Ngo ST, Steyn FJ and McCombe PA. Gender differences in autoimmune disease. Front Neuroendocrinol 2014; 35: 347–369.  [Link]
42.
Babickova J, et al. Sex differences in experimentally induced colitis in mice: a role for estrogens. Inflammation 2015; 38: 1996–2006.  [Link]
43.
te Velde AA, et al. Effects of dietary plant sterols and stanol esters with low- and high-fat diets in chronic and acute models for experimental colitis. Nutrients 2015; 7: 8518–8531.  [Link]
44.
Berglund M, et al. Gender dependent importance of IRAK-1 in dextran sulfate sodium induced colitis. Cell Immunol 2009; 259: 27–32.  [Link]
45.
Alex P, et al. Distinct cytokine patterns identified from multiplex profiles of murine DSS and TNBS-induced colitis. Inflamm Bowel Dis 2009; 15: 341–352.  [Link]
46.
Gonder JC and Laber K. A renewed look at laboratory rodent housing and management. ILAR J 2007; 48: 29–36.  [Link]
47.
Bramhall M, et al. Quality of methods reporting in animal models of colitis. Inflamm Bowel Dis 2015; 21: 1248–1259.  [Link]
48.
Kilkenny C, et al. Improving bioscience research reporting: the ARRIVE guidelines for reporting animal research. PLoS Biol 2010; 8: e1000412.  [Link]
49.
Koboziev I, et al. Pharmacological intervention studies using mouse models of the inflammatory bowel diseases: translating preclinical data into new drug therapies. Inflamm Bowel Dis 2011; 17: 1229–1245.  [Link]
50.
Koelink PJ, Wildenberg ME, Stitt LW, Feagan BG, Koldijk M, Van ‘T Wout AB, et al. Development of Reliable, Valid and Responsive Scoring Systems for Endoscopy and Histology in Animal Models for Inflammatory Bowel Disease. Journal of Crohn’s and Colitis. 2018 Jun 28;12(7):794–803.
51.
[url:https://academic.oup.com/ecco-jcc/article/12/7/794/4955731?login=false]
52.
Valatas V, Vakas M and Kolios G. The value of experimental models of colitis in predicting efficacy of biological therapies for inflammatory bowel diseases. Am J Physiol Gastrointest Liver Physiol 2013; 305: G763–G785.  [Link]
53.
Prattis S and Jurjus A. Spontaneous and transgenic rodent models of inflammatory bowel disease. Lab Anim Res 2015; 31: 47–68.  [Link]

Abstract

Nowadays, obesity represents an immense burden for global healthcare. The number of overweight or obese cases has exceeded that of underweight individuals.1 Bariatric surgery is accepted as a safe and effective treatment for patients with morbid obesity and has gained widespread popularity in the past two decades. Advancements in surgical techniques, perioperative care, and fellowship-based bariatric surgery training have substantially reduced morbidity and mortality rates. Nevertheless, several controversial aspects of surgical treatments of morbidly obese patients are still to be considered. Here we discuss the mistakes made when managing patients who are candidates for or have been submitted to bariatric surgery in the preoperative, perioperative, and postoperative periods. As high-level evidence is lacking for many aspects of surgical bariatric care, the discussion is based on our long-standing clinical experience.


Topics

Primary Care Small Intestine & Nutrition Surgery

Citation

Papadia Saverio F and Camerini G. Mistakes in bariatric surgery and how to avoid them. UEG Education 2022; 22: 11–15.

Published

2022

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Mistakes in short bowel and how to avoid them

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Kestutis Adamonis Kestutis Adamonis, Stéphanie O Breukink, Sadé L Assmann

UEG Mistakes In Articles
Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

Log in to continue.

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Log In Create a free account

Not sure what you can access? Learn more about account types.

Mistakes in the management of carbohydrate intolerance and how to avoid them

Johann Hammer, Heinz Florian Hammer, Mark Fox

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

This summary was generated by an AI large language model based on the content transcript. It is for informational purposes only and should not be considered a substitute for clinical judgment. Always rely on your professional expertise and the full clinical context when making clinical decisions.

References

Mistakes
References
Mistake 1 Mistake 2 Mistake 3 Mistake 4 Mistake 5 Mistake 6 Mistake 7 Mistake 8 Mistake 9 Mistake 10
1.
Bouma G and Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol 2003; 3: 521–533.  [Link]
2.
Khanna PV, et al. Use of animal models in elucidating disease pathogenesis in IBD. Semin Immunopathol 2014; 36: 541–551.  [Link]
3.
Mizoguchi A and Mizoguchi E. Animal models of IBD: linkage to human disease. Curr Opin Pharmacol 2010; 10: 578–587.  [Link]
4.
Uhlig HH and Powrie F. Mouse models of intestinal inflammation as tools to understand the pathogenesis of inflammatory bowel disease. Eur J Immunol 2009; 39: 2021–2026.  [Link]
5.
Zeeff SB, Kunne C, Bouma G, et al. Actual usage and quality of experimental colitis models in preclinical efficacy testing: a scoping review. Inflamm Bowel Dis Prepublished April 21, 20016, DOI: 10.1097/MIB.0000000000000758.  [Link]
6.
DeVoss J and Diehl L. Murine models of inflammatory bowel disease (IBD): challenges of modeling human disease. Toxicol Pathol 2014; 42: 99–110.  [Link]
7.
Goyal N, et al. Animal models of inflammatory bowel disease: a review. Inflammopharmacology 2014; 22: 219–33. [Link]
8.
Jones-Hall YL and Grisham MB. Immunopathological characterization of selected mouse models of inflammatory bowel disease: Comparison to human disease. Pathophysiology 2014; 21: 267–88.  [Link]
9.
te Velde AA, et al. Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease. Inflamm Bowel Dis 2007; 13: 325–330.  [Link]
10.
te Velde AA, Verstege MI and Hommes DW. Critical appraisal of the current practice in murine TNBS-induced colitis. Inflamm Bowel Dis 2006; 12: 995–999.  [Link]
11.
Wirtz S, et al. Chemically induced mouse models of intestinal inflammation. Nat Protoc 2007; 2: 541–546.  [Link]
12.
Read S and Powrie F. Induction of inflammatory bowel disease in immunodeficient mice by depletion of regulatory T cells. Curr Protoc Immunol 1999; 30 (suppl): 15.13.1–15.13.10.  [Link]
13.
Ostanin DV, et al. T cell transfer model of chronic colitis: concepts, considerations, and tricks of the trade. Am J Physiol Gastrointest Liver Physiol 2009; 296: G135–G146.  [Link]
14.
National Academies of Sciences, Engineering, and Medicine. Reproducibility Issues in Research with Animals and Animal Models: Workshop in Brief. Washington, DC: The National Academies Press, 2015.
15.
Prinz F, Schlange T and Asadullah K. Believe it or not: how much can we rely on published data on potential drug targets? Nat Rev Drug Discov 2011; 10: 712.  [Link]
16.
Nature. Chow down. Nature 2016; 530: 254.  [Link]
17.
Reardon S. A mouse's house may ruin experiments. Nature 2016; 530: 264.  [Link]
18.
Gkouskou KK, et al. The gut microbiota in mouse models of inflammatory bowel disease. Front Cell Infect Microbiol 2014; 4: 28.  [Link]
19.
Macpherson AJ and McCoy KD. Standardised animal models of host microbial mutualism. Mucosal Immunol 2015; 8: 476–486.  [Link]
20.
Hooijmans CR, et al. SYRCLE's risk of bias tool for animal studies. BMC Med Res Methodol 2014; 14: 43.  [Link]
21.
Erben U, et al. A guide to histomorphological evaluation of intestinal inflammation in mouse models. Int J Clin Exp Pathol 2014; 7: 4557–4576.  [Link]
22.
Gibson-Corley KN, Olivier AK and Meyerholz DK.  Principles for valid histopathologic scoring in research. Vet Pathol 2013; 50: 1007–1015.  [Link]
23.
Hansen AK, et al. Impact of the gut microbiota on rodent models of human disease. World J Gastroenterol 2014; 20: 17727–17736.  [Link]
24.
Schoeb TR and Bullard DC. Microbial and histopathologic considerations in the use of mouse models of inflammatory bowel diseases. Inflamm Bowel Dis 2012; 18: 1558–1565.  [Link]
25.
Hansen AK, et al. A review of applied aspects of dealing with gut microbiota impact on rodent models. ILAR J, 2015; 56: 250–264.  [Link]
26.
Jakobsson HE, et al. The composition of the gut microbiota shapes the colon mucus barrier. EMBO Rep 2015; 16: 164–177.  [Link]
27.
Ivanov II, et al. Induction of intestinal Th17 cells by segmented filamentous bacteria. Cell 2009; 139: 485–498.  [Link]
28.
Ericsson AC, et al. Effects of vendor and genetic background on the composition of the fecal microbiota of inbred mice. PLoS One 2015: 10: e0116704.  [Link]
29.
Zenewicz LA, et al. IL-22 deficiency alters colonoc microbiota to be transmissable and colitogenic. J Immunol 2013; 190: 5306–5312.  [Link]
30.
Mahler M, et al. Differential susceptibility of inbred mouse strains to dextran sulfate sodium-induced colitis. Am J Physiol 1998; 274: G544–G551.  [Link]
31.
Melgar S, Karlsson A and Michaelsson E. Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation. Am J Physiol Gastrointest Liver Physiol 2005; 288: G1328–G1338.  [Link]
32.
Scheiffele F and Fuss IJ. Induction of TNBS colitis in mice. Curr Protoc Immunol 2002; Chapter 15: Unit 15.19.  [Link]
33.
Bouma G, Kaushiva A and Strober W. Experimental murine colitis is regulated by two genetic loci, including one on chromosome 11 that regulates IL-12 responses. Gastroenterology 2002; 123: 554–565.  [Link]
34.
Hsieh CS, et al. T cell genetic background determines default T helper phenotype development in vitro. J Exp Med 1995; 181: 713–721.  [Link]
35.
Powrie F, et al. Inhibition of Th1 responses prevents inflammatory bowel disease in scid mice reconstituted with CD45RBhi CD4+ T cells. Immunity 1994; 1: 553–562.  [Link]
36.
Berg DJ, et al. Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses. J Clin Invest 1996; 98: 1010–1020.  [Link]
37.
Beckwith J, et al. Cdcs1, a major colitogenic locus in mice, regulates innate and adaptive immune response to enteric bacterial antigens. Gastroenterology 2005; 129: 1473–1484.  [Link]
38.
Holgersen K, et al. Characterisation of enterocolitis in the piroxicam-accelerated interleukin-10 knock out mouse—a model mimicking inflammatory bowel disease. J Crohns Colitis 2014; 8: 147–160.  [Link]
39.
Atamni HJ, et al. High-fat-diet induced development of increased fasting glucose levels and impaired response to intraperitoneal glucose challenge in the collaborative cross mouse genetic reference population. BMC Genet 2016; 17: 10.  [Link]
40.
Aylor DL, et al. Genetic analysis of complex traits in the emerging Collaborative Cross. Genome Res 2011; 21:  1213–1222.  [Link]
41.
Ngo ST, Steyn FJ and McCombe PA. Gender differences in autoimmune disease. Front Neuroendocrinol 2014; 35: 347–369.  [Link]
42.
Babickova J, et al. Sex differences in experimentally induced colitis in mice: a role for estrogens. Inflammation 2015; 38: 1996–2006.  [Link]
43.
te Velde AA, et al. Effects of dietary plant sterols and stanol esters with low- and high-fat diets in chronic and acute models for experimental colitis. Nutrients 2015; 7: 8518–8531.  [Link]
44.
Berglund M, et al. Gender dependent importance of IRAK-1 in dextran sulfate sodium induced colitis. Cell Immunol 2009; 259: 27–32.  [Link]
45.
Alex P, et al. Distinct cytokine patterns identified from multiplex profiles of murine DSS and TNBS-induced colitis. Inflamm Bowel Dis 2009; 15: 341–352.  [Link]
46.
Gonder JC and Laber K. A renewed look at laboratory rodent housing and management. ILAR J 2007; 48: 29–36.  [Link]
47.
Bramhall M, et al. Quality of methods reporting in animal models of colitis. Inflamm Bowel Dis 2015; 21: 1248–1259.  [Link]
48.
Kilkenny C, et al. Improving bioscience research reporting: the ARRIVE guidelines for reporting animal research. PLoS Biol 2010; 8: e1000412.  [Link]
49.
Koboziev I, et al. Pharmacological intervention studies using mouse models of the inflammatory bowel diseases: translating preclinical data into new drug therapies. Inflamm Bowel Dis 2011; 17: 1229–1245.  [Link]
50.
Koelink PJ, Wildenberg ME, Stitt LW, Feagan BG, Koldijk M, Van ‘T Wout AB, et al. Development of Reliable, Valid and Responsive Scoring Systems for Endoscopy and Histology in Animal Models for Inflammatory Bowel Disease. Journal of Crohn’s and Colitis. 2018 Jun 28;12(7):794–803.
51.
[url:https://academic.oup.com/ecco-jcc/article/12/7/794/4955731?login=false]
52.
Valatas V, Vakas M and Kolios G. The value of experimental models of colitis in predicting efficacy of biological therapies for inflammatory bowel diseases. Am J Physiol Gastrointest Liver Physiol 2013; 305: G763–G785.  [Link]
53.
Prattis S and Jurjus A. Spontaneous and transgenic rodent models of inflammatory bowel disease. Lab Anim Res 2015; 31: 47–68.  [Link]

Abstract

Carbohydrates not absorbed in the small intestine are fermented by colonic bacteria to organic acids and gases(e.g. carbon dioxide, hydrogen and methane), part of which is absorbed in the colon, the other part remaining in the lumen. Large interindividual differences have been demonstrated for the production of such acids and gas. Carbohydrate malabsorption can be diagnosed by using the hydrogen breath test, because the gases produced after administration of a provocative dose of carbohydrate are unique products of bacterial carbohydrate fermentation.

Topics

Small Intestine & Nutrition

Citation

Hammer HF, Hammer J and Fox M. Mistakes in the management of carbohydrate intolerance and how to avoid them. UEG Education 2019; 19: 9–14

Published

2019

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UEG Mistakes In Articles
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Mistakes in rumination syndrome and how to avoid them

Alberto Ezquerra-Durán, Elizabeth Barba Orozco

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

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Thanks for your feedback.

This summary was generated by an AI large language model based on the content transcript. It is for informational purposes only and should not be considered a substitute for clinical judgment. Always rely on your professional expertise and the full clinical context when making clinical decisions.

References

Mistakes
References
Mistake 1 Mistake 2 Mistake 3 Mistake 4 Mistake 5 Mistake 6 Mistake 7 Mistake 8 Mistake 9 Mistake 10
1.
Bouma G and Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol 2003; 3: 521–533.  [Link]
2.
Khanna PV, et al. Use of animal models in elucidating disease pathogenesis in IBD. Semin Immunopathol 2014; 36: 541–551.  [Link]
3.
Mizoguchi A and Mizoguchi E. Animal models of IBD: linkage to human disease. Curr Opin Pharmacol 2010; 10: 578–587.  [Link]
4.
Uhlig HH and Powrie F. Mouse models of intestinal inflammation as tools to understand the pathogenesis of inflammatory bowel disease. Eur J Immunol 2009; 39: 2021–2026.  [Link]
5.
Zeeff SB, Kunne C, Bouma G, et al. Actual usage and quality of experimental colitis models in preclinical efficacy testing: a scoping review. Inflamm Bowel Dis Prepublished April 21, 20016, DOI: 10.1097/MIB.0000000000000758.  [Link]
6.
DeVoss J and Diehl L. Murine models of inflammatory bowel disease (IBD): challenges of modeling human disease. Toxicol Pathol 2014; 42: 99–110.  [Link]
7.
Goyal N, et al. Animal models of inflammatory bowel disease: a review. Inflammopharmacology 2014; 22: 219–33. [Link]
8.
Jones-Hall YL and Grisham MB. Immunopathological characterization of selected mouse models of inflammatory bowel disease: Comparison to human disease. Pathophysiology 2014; 21: 267–88.  [Link]
9.
te Velde AA, et al. Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease. Inflamm Bowel Dis 2007; 13: 325–330.  [Link]
10.
te Velde AA, Verstege MI and Hommes DW. Critical appraisal of the current practice in murine TNBS-induced colitis. Inflamm Bowel Dis 2006; 12: 995–999.  [Link]
11.
Wirtz S, et al. Chemically induced mouse models of intestinal inflammation. Nat Protoc 2007; 2: 541–546.  [Link]
12.
Read S and Powrie F. Induction of inflammatory bowel disease in immunodeficient mice by depletion of regulatory T cells. Curr Protoc Immunol 1999; 30 (suppl): 15.13.1–15.13.10.  [Link]
13.
Ostanin DV, et al. T cell transfer model of chronic colitis: concepts, considerations, and tricks of the trade. Am J Physiol Gastrointest Liver Physiol 2009; 296: G135–G146.  [Link]
14.
National Academies of Sciences, Engineering, and Medicine. Reproducibility Issues in Research with Animals and Animal Models: Workshop in Brief. Washington, DC: The National Academies Press, 2015.
15.
Prinz F, Schlange T and Asadullah K. Believe it or not: how much can we rely on published data on potential drug targets? Nat Rev Drug Discov 2011; 10: 712.  [Link]
16.
Nature. Chow down. Nature 2016; 530: 254.  [Link]
17.
Reardon S. A mouse's house may ruin experiments. Nature 2016; 530: 264.  [Link]
18.
Gkouskou KK, et al. The gut microbiota in mouse models of inflammatory bowel disease. Front Cell Infect Microbiol 2014; 4: 28.  [Link]
19.
Macpherson AJ and McCoy KD. Standardised animal models of host microbial mutualism. Mucosal Immunol 2015; 8: 476–486.  [Link]
20.
Hooijmans CR, et al. SYRCLE's risk of bias tool for animal studies. BMC Med Res Methodol 2014; 14: 43.  [Link]
21.
Erben U, et al. A guide to histomorphological evaluation of intestinal inflammation in mouse models. Int J Clin Exp Pathol 2014; 7: 4557–4576.  [Link]
22.
Gibson-Corley KN, Olivier AK and Meyerholz DK.  Principles for valid histopathologic scoring in research. Vet Pathol 2013; 50: 1007–1015.  [Link]
23.
Hansen AK, et al. Impact of the gut microbiota on rodent models of human disease. World J Gastroenterol 2014; 20: 17727–17736.  [Link]
24.
Schoeb TR and Bullard DC. Microbial and histopathologic considerations in the use of mouse models of inflammatory bowel diseases. Inflamm Bowel Dis 2012; 18: 1558–1565.  [Link]
25.
Hansen AK, et al. A review of applied aspects of dealing with gut microbiota impact on rodent models. ILAR J, 2015; 56: 250–264.  [Link]
26.
Jakobsson HE, et al. The composition of the gut microbiota shapes the colon mucus barrier. EMBO Rep 2015; 16: 164–177.  [Link]
27.
Ivanov II, et al. Induction of intestinal Th17 cells by segmented filamentous bacteria. Cell 2009; 139: 485–498.  [Link]
28.
Ericsson AC, et al. Effects of vendor and genetic background on the composition of the fecal microbiota of inbred mice. PLoS One 2015: 10: e0116704.  [Link]
29.
Zenewicz LA, et al. IL-22 deficiency alters colonoc microbiota to be transmissable and colitogenic. J Immunol 2013; 190: 5306–5312.  [Link]
30.
Mahler M, et al. Differential susceptibility of inbred mouse strains to dextran sulfate sodium-induced colitis. Am J Physiol 1998; 274: G544–G551.  [Link]
31.
Melgar S, Karlsson A and Michaelsson E. Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation. Am J Physiol Gastrointest Liver Physiol 2005; 288: G1328–G1338.  [Link]
32.
Scheiffele F and Fuss IJ. Induction of TNBS colitis in mice. Curr Protoc Immunol 2002; Chapter 15: Unit 15.19.  [Link]
33.
Bouma G, Kaushiva A and Strober W. Experimental murine colitis is regulated by two genetic loci, including one on chromosome 11 that regulates IL-12 responses. Gastroenterology 2002; 123: 554–565.  [Link]
34.
Hsieh CS, et al. T cell genetic background determines default T helper phenotype development in vitro. J Exp Med 1995; 181: 713–721.  [Link]
35.
Powrie F, et al. Inhibition of Th1 responses prevents inflammatory bowel disease in scid mice reconstituted with CD45RBhi CD4+ T cells. Immunity 1994; 1: 553–562.  [Link]
36.
Berg DJ, et al. Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses. J Clin Invest 1996; 98: 1010–1020.  [Link]
37.
Beckwith J, et al. Cdcs1, a major colitogenic locus in mice, regulates innate and adaptive immune response to enteric bacterial antigens. Gastroenterology 2005; 129: 1473–1484.  [Link]
38.
Holgersen K, et al. Characterisation of enterocolitis in the piroxicam-accelerated interleukin-10 knock out mouse—a model mimicking inflammatory bowel disease. J Crohns Colitis 2014; 8: 147–160.  [Link]
39.
Atamni HJ, et al. High-fat-diet induced development of increased fasting glucose levels and impaired response to intraperitoneal glucose challenge in the collaborative cross mouse genetic reference population. BMC Genet 2016; 17: 10.  [Link]
40.
Aylor DL, et al. Genetic analysis of complex traits in the emerging Collaborative Cross. Genome Res 2011; 21:  1213–1222.  [Link]
41.
Ngo ST, Steyn FJ and McCombe PA. Gender differences in autoimmune disease. Front Neuroendocrinol 2014; 35: 347–369.  [Link]
42.
Babickova J, et al. Sex differences in experimentally induced colitis in mice: a role for estrogens. Inflammation 2015; 38: 1996–2006.  [Link]
43.
te Velde AA, et al. Effects of dietary plant sterols and stanol esters with low- and high-fat diets in chronic and acute models for experimental colitis. Nutrients 2015; 7: 8518–8531.  [Link]
44.
Berglund M, et al. Gender dependent importance of IRAK-1 in dextran sulfate sodium induced colitis. Cell Immunol 2009; 259: 27–32.  [Link]
45.
Alex P, et al. Distinct cytokine patterns identified from multiplex profiles of murine DSS and TNBS-induced colitis. Inflamm Bowel Dis 2009; 15: 341–352.  [Link]
46.
Gonder JC and Laber K. A renewed look at laboratory rodent housing and management. ILAR J 2007; 48: 29–36.  [Link]
47.
Bramhall M, et al. Quality of methods reporting in animal models of colitis. Inflamm Bowel Dis 2015; 21: 1248–1259.  [Link]
48.
Kilkenny C, et al. Improving bioscience research reporting: the ARRIVE guidelines for reporting animal research. PLoS Biol 2010; 8: e1000412.  [Link]
49.
Koboziev I, et al. Pharmacological intervention studies using mouse models of the inflammatory bowel diseases: translating preclinical data into new drug therapies. Inflamm Bowel Dis 2011; 17: 1229–1245.  [Link]
50.
Koelink PJ, Wildenberg ME, Stitt LW, Feagan BG, Koldijk M, Van ‘T Wout AB, et al. Development of Reliable, Valid and Responsive Scoring Systems for Endoscopy and Histology in Animal Models for Inflammatory Bowel Disease. Journal of Crohn’s and Colitis. 2018 Jun 28;12(7):794–803.
51.
[url:https://academic.oup.com/ecco-jcc/article/12/7/794/4955731?login=false]
52.
Valatas V, Vakas M and Kolios G. The value of experimental models of colitis in predicting efficacy of biological therapies for inflammatory bowel diseases. Am J Physiol Gastrointest Liver Physiol 2013; 305: G763–G785.  [Link]
53.
Prattis S and Jurjus A. Spontaneous and transgenic rodent models of inflammatory bowel disease. Lab Anim Res 2015; 31: 47–68.  [Link]

Abstract

Topics

Neurogastroenterology & Motility

Citation

Ezquerra-Durán A and Barba-Orozco E. Mistakes in rumination syndrome and how to avoid them. UEG Education 2025; 25: 10-13.

Published

2025

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UEG Mistakes In Articles
Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

Log in to continue.

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Log In Create a free account

Not sure what you can access? Learn more about account types.

Mistakes in faecal incontinence management and how to avoid them

Kestutis Adamonis, Sadé L Assmann, Stéphanie O Breukink

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

This summary was generated by an AI large language model based on the content transcript. It is for informational purposes only and should not be considered a substitute for clinical judgment. Always rely on your professional expertise and the full clinical context when making clinical decisions.

References

Mistakes
References
Mistake 1 Mistake 2 Mistake 3 Mistake 4 Mistake 5 Mistake 6 Mistake 7 Mistake 8 Mistake 9 Mistake 10
1.
Bouma G and Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol 2003; 3: 521–533.  [Link]
2.
Khanna PV, et al. Use of animal models in elucidating disease pathogenesis in IBD. Semin Immunopathol 2014; 36: 541–551.  [Link]
3.
Mizoguchi A and Mizoguchi E. Animal models of IBD: linkage to human disease. Curr Opin Pharmacol 2010; 10: 578–587.  [Link]
4.
Uhlig HH and Powrie F. Mouse models of intestinal inflammation as tools to understand the pathogenesis of inflammatory bowel disease. Eur J Immunol 2009; 39: 2021–2026.  [Link]
5.
Zeeff SB, Kunne C, Bouma G, et al. Actual usage and quality of experimental colitis models in preclinical efficacy testing: a scoping review. Inflamm Bowel Dis Prepublished April 21, 20016, DOI: 10.1097/MIB.0000000000000758.  [Link]
6.
DeVoss J and Diehl L. Murine models of inflammatory bowel disease (IBD): challenges of modeling human disease. Toxicol Pathol 2014; 42: 99–110.  [Link]
7.
Goyal N, et al. Animal models of inflammatory bowel disease: a review. Inflammopharmacology 2014; 22: 219–33. [Link]
8.
Jones-Hall YL and Grisham MB. Immunopathological characterization of selected mouse models of inflammatory bowel disease: Comparison to human disease. Pathophysiology 2014; 21: 267–88.  [Link]
9.
te Velde AA, et al. Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease. Inflamm Bowel Dis 2007; 13: 325–330.  [Link]
10.
te Velde AA, Verstege MI and Hommes DW. Critical appraisal of the current practice in murine TNBS-induced colitis. Inflamm Bowel Dis 2006; 12: 995–999.  [Link]
11.
Wirtz S, et al. Chemically induced mouse models of intestinal inflammation. Nat Protoc 2007; 2: 541–546.  [Link]
12.
Read S and Powrie F. Induction of inflammatory bowel disease in immunodeficient mice by depletion of regulatory T cells. Curr Protoc Immunol 1999; 30 (suppl): 15.13.1–15.13.10.  [Link]
13.
Ostanin DV, et al. T cell transfer model of chronic colitis: concepts, considerations, and tricks of the trade. Am J Physiol Gastrointest Liver Physiol 2009; 296: G135–G146.  [Link]
14.
National Academies of Sciences, Engineering, and Medicine. Reproducibility Issues in Research with Animals and Animal Models: Workshop in Brief. Washington, DC: The National Academies Press, 2015.
15.
Prinz F, Schlange T and Asadullah K. Believe it or not: how much can we rely on published data on potential drug targets? Nat Rev Drug Discov 2011; 10: 712.  [Link]
16.
Nature. Chow down. Nature 2016; 530: 254.  [Link]
17.
Reardon S. A mouse's house may ruin experiments. Nature 2016; 530: 264.  [Link]
18.
Gkouskou KK, et al. The gut microbiota in mouse models of inflammatory bowel disease. Front Cell Infect Microbiol 2014; 4: 28.  [Link]
19.
Macpherson AJ and McCoy KD. Standardised animal models of host microbial mutualism. Mucosal Immunol 2015; 8: 476–486.  [Link]
20.
Hooijmans CR, et al. SYRCLE's risk of bias tool for animal studies. BMC Med Res Methodol 2014; 14: 43.  [Link]
21.
Erben U, et al. A guide to histomorphological evaluation of intestinal inflammation in mouse models. Int J Clin Exp Pathol 2014; 7: 4557–4576.  [Link]
22.
Gibson-Corley KN, Olivier AK and Meyerholz DK.  Principles for valid histopathologic scoring in research. Vet Pathol 2013; 50: 1007–1015.  [Link]
23.
Hansen AK, et al. Impact of the gut microbiota on rodent models of human disease. World J Gastroenterol 2014; 20: 17727–17736.  [Link]
24.
Schoeb TR and Bullard DC. Microbial and histopathologic considerations in the use of mouse models of inflammatory bowel diseases. Inflamm Bowel Dis 2012; 18: 1558–1565.  [Link]
25.
Hansen AK, et al. A review of applied aspects of dealing with gut microbiota impact on rodent models. ILAR J, 2015; 56: 250–264.  [Link]
26.
Jakobsson HE, et al. The composition of the gut microbiota shapes the colon mucus barrier. EMBO Rep 2015; 16: 164–177.  [Link]
27.
Ivanov II, et al. Induction of intestinal Th17 cells by segmented filamentous bacteria. Cell 2009; 139: 485–498.  [Link]
28.
Ericsson AC, et al. Effects of vendor and genetic background on the composition of the fecal microbiota of inbred mice. PLoS One 2015: 10: e0116704.  [Link]
29.
Zenewicz LA, et al. IL-22 deficiency alters colonoc microbiota to be transmissable and colitogenic. J Immunol 2013; 190: 5306–5312.  [Link]
30.
Mahler M, et al. Differential susceptibility of inbred mouse strains to dextran sulfate sodium-induced colitis. Am J Physiol 1998; 274: G544–G551.  [Link]
31.
Melgar S, Karlsson A and Michaelsson E. Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation. Am J Physiol Gastrointest Liver Physiol 2005; 288: G1328–G1338.  [Link]
32.
Scheiffele F and Fuss IJ. Induction of TNBS colitis in mice. Curr Protoc Immunol 2002; Chapter 15: Unit 15.19.  [Link]
33.
Bouma G, Kaushiva A and Strober W. Experimental murine colitis is regulated by two genetic loci, including one on chromosome 11 that regulates IL-12 responses. Gastroenterology 2002; 123: 554–565.  [Link]
34.
Hsieh CS, et al. T cell genetic background determines default T helper phenotype development in vitro. J Exp Med 1995; 181: 713–721.  [Link]
35.
Powrie F, et al. Inhibition of Th1 responses prevents inflammatory bowel disease in scid mice reconstituted with CD45RBhi CD4+ T cells. Immunity 1994; 1: 553–562.  [Link]
36.
Berg DJ, et al. Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses. J Clin Invest 1996; 98: 1010–1020.  [Link]
37.
Beckwith J, et al. Cdcs1, a major colitogenic locus in mice, regulates innate and adaptive immune response to enteric bacterial antigens. Gastroenterology 2005; 129: 1473–1484.  [Link]
38.
Holgersen K, et al. Characterisation of enterocolitis in the piroxicam-accelerated interleukin-10 knock out mouse—a model mimicking inflammatory bowel disease. J Crohns Colitis 2014; 8: 147–160.  [Link]
39.
Atamni HJ, et al. High-fat-diet induced development of increased fasting glucose levels and impaired response to intraperitoneal glucose challenge in the collaborative cross mouse genetic reference population. BMC Genet 2016; 17: 10.  [Link]
40.
Aylor DL, et al. Genetic analysis of complex traits in the emerging Collaborative Cross. Genome Res 2011; 21:  1213–1222.  [Link]
41.
Ngo ST, Steyn FJ and McCombe PA. Gender differences in autoimmune disease. Front Neuroendocrinol 2014; 35: 347–369.  [Link]
42.
Babickova J, et al. Sex differences in experimentally induced colitis in mice: a role for estrogens. Inflammation 2015; 38: 1996–2006.  [Link]
43.
te Velde AA, et al. Effects of dietary plant sterols and stanol esters with low- and high-fat diets in chronic and acute models for experimental colitis. Nutrients 2015; 7: 8518–8531.  [Link]
44.
Berglund M, et al. Gender dependent importance of IRAK-1 in dextran sulfate sodium induced colitis. Cell Immunol 2009; 259: 27–32.  [Link]
45.
Alex P, et al. Distinct cytokine patterns identified from multiplex profiles of murine DSS and TNBS-induced colitis. Inflamm Bowel Dis 2009; 15: 341–352.  [Link]
46.
Gonder JC and Laber K. A renewed look at laboratory rodent housing and management. ILAR J 2007; 48: 29–36.  [Link]
47.
Bramhall M, et al. Quality of methods reporting in animal models of colitis. Inflamm Bowel Dis 2015; 21: 1248–1259.  [Link]
48.
Kilkenny C, et al. Improving bioscience research reporting: the ARRIVE guidelines for reporting animal research. PLoS Biol 2010; 8: e1000412.  [Link]
49.
Koboziev I, et al. Pharmacological intervention studies using mouse models of the inflammatory bowel diseases: translating preclinical data into new drug therapies. Inflamm Bowel Dis 2011; 17: 1229–1245.  [Link]
50.
Koelink PJ, Wildenberg ME, Stitt LW, Feagan BG, Koldijk M, Van ‘T Wout AB, et al. Development of Reliable, Valid and Responsive Scoring Systems for Endoscopy and Histology in Animal Models for Inflammatory Bowel Disease. Journal of Crohn’s and Colitis. 2018 Jun 28;12(7):794–803.
51.
[url:https://academic.oup.com/ecco-jcc/article/12/7/794/4955731?login=false]
52.
Valatas V, Vakas M and Kolios G. The value of experimental models of colitis in predicting efficacy of biological therapies for inflammatory bowel diseases. Am J Physiol Gastrointest Liver Physiol 2013; 305: G763–G785.  [Link]
53.
Prattis S and Jurjus A. Spontaneous and transgenic rodent models of inflammatory bowel disease. Lab Anim Res 2015; 31: 47–68.  [Link]

Abstract

People with faecal incontinence (FI) suffer from chronic involuntary loss of bowel content. Patients often experience embarrassment, shame, low self-esteem, and depression, affecting their quality of life. Treatment approaches vary, and less invasive options should be tried before considering more invasive treatments. It's important to consider contributing factors, physician and patient preferences, and available procedures. This article discusses common mistakes in treating faecal incontinence and how to avoid them, based on evidence and clinical experience.

Topics

Neurogastroenterology & Motility

Citation

Assmann S L, Breukink S O and Keszthelyi D. Mistakes in faecal incontinence management and how to avoid them. UEG Education 2023; 23: 1-3.

Published

2023

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