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SYSTEMIC ANTIBODY RESPONSES AGAINST GUT MICROBIOTA FLAGELLINS IMPLICATE SHARED AND DIVERGENT IMMUNE REACTIVITY IN CROHN'S DISEASE AND CHRONIC FATIGUE SYNDROME

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Introduction

Patients with Crohn’s disease (CD) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) exhibit elevated antibody responses against gut microbiota flagellins. However, flagellin-specific antibody repertoires and functional roles in the diseases remain incompletely understood. Bacterial flagellins can be categorized into three types depending on their interaction with toll-like receptor 5 (TLR5): (1) "stimulator" and (2) "silent" flagellins, binding TLR5 through a conserved N-terminal motif, with only stimulators activating TLR5 due to a specific C-terminal domain; (3) "evader" flagellins of pathogens, which circumvent TLR5 activation via mutated N-terminal TLR5 binding motifs. Here we studied the characteristics, epitope binding, and sequence (dis)similarity of anti-flagellin antibody responses in CD and ME/CFS.

Aims & Methods

Since conventional antibody profiling methods like enzyme-linked immunosorbent assays [ELISAs] do not allow for large-scale measurements of antibody repertoires, we leveraged phage-display immunoprecipitation sequencing (PhIP-Seq) to characterize 344,000 rationally selected peptide antigens in 256 patients with CD, 40 patients with ME/CFS and in two equally sized groups of age- and sex-matched healthy controls from population-based cohorts in the Netherlands and U.K., respectively. Different sequence alignment strategies were employed to compare flagellin peptide structures with observed antibody-bound flagellin peptide reactivity.

Results

Both patients with CD and ME/CFS exhibited elevated antibody responses against distinct regions of flagellin peptides compared to healthy individuals (P<0.001). N-terminal binding to Lachnospiraceae flagellins was comparable in both diseases, while C-terminal binding was more prevalent in CD. N-terminal antibody-bound flagellin sequences were similar across CD and ME/CFS, resembling ‘stimulator’ and ‘silent’ flagellins more than evaders. However, C-terminal antibody-bound flagellins showed higher resemblance to stimulator than to silent flagellins in CD, but not in ME/CFS. This group of antibody-bound flagellins was exclusively identified in a subset (10-20%) of patients with CD and characterized by its strong overrepresentation (exceeding 20-fold), underscoring its potential significance in distinguishing pathophysiologic subtypes of CD.

Conclusion

Antibody binding to the N-terminal domain of stimulator and silent flagellins may impact TLR5 activation in both CD and ME/CFS patients. Furthermore, elevated antibody binding to the C-terminal domain of stimulator flagellins in CD may explain pathophysiological differences between diseases. Our results highlight the diagnostic potential of these antibody responses and their impact on innate/adaptive immunity balance.

SYSTEMIC ANTIBODY RESPONSES AGAINST GUT MICROBIOTA FLAGELLINS IMPLICATE SHARED AND DIVERGENT IMMUNE REACTIVITY IN CROHN'S DISEASE AND CHRONIC FATIGUE SYNDROME

Arno R. Bourgonje 1, Nicolai Hörstke 2, Michaela Fehringer 2, Gabriel Innocenti 2, Thomas Vogl 2

1 University Medical Center Groningen, Groningen, Netherlands|||Icahn School of Medicine at Mount Sinai, New York, United States

2 Medical University of Vienna, Vienna, Austria

Event

UEG Week Vienna 2024

Topics

Gut Microbiota IBD Immunology

Submission format

Abstract

Session

Understanding disease primers of IBD: Part 2

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Panel discussion: Liver and pregnancy - Beware of dangerous liaisons

Event

UEG Postgraduate Teaching Programme Berlin 2025

Topics

Hepatobiliary Paediatrics

Session

Liver and pregnancy: Beware of dangerous liaisons

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Introduction Mistakes in…: Lower GI

Henriette Heinrich 1

1 Stadtspital Triemli, Zürich, Switzerland

Event

UEG Week Berlin 2025

Topics

Colorectal Endoscopy IBD Nurses

Session

Mistakes in…: Lower GI

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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PREVALENCE, ETIOLOGY AND OUTCOME OF ACUTE PANCREATITIS IN INFLAMMATORY BOWEL DISEASE: EUROPEAN PANDORA STUDY

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Introduction

Although an increased risk of acute pancreatitis (AP) in inflammatory bowel disease (IBD) has been previously described, there are only small series, and data on clinical management are lacking. We aimed to investigate the prevalence, etiology, and outcome of AP in IBD patients, including management, in a multicenter international study.

Aims & Methods

A two-step retrospective study was conducted involving 34 centers across Europe. The first step consisted of a survey questionnaire examining the number of AP (according to the Atlanta criteria) in adult IBD patients observed during a 10-year study period (2011-2020), and the second one in collecting data on IBD characteristics, onset of AP, etiology, clinical management, and outcome. The study's primary aim was to estimate the prevalence of AP in IBD patients based on the total number of IBD patients observed in the study period indicated in the survey form. Secondary aims included investigating the etiology of AP in IBD patients, the relationship between IBD medications and AP, the role of different imaging modalities in improving the diagnosis of pancreatic abnormalities, and the clinical outcome of AP. The study protocol has been disseminated through the ECCO (European Crohn’s and Colitis Organization) platform after review and support by Clinical Research Committee.

Results

The expected prevalence of AP in IBD patients, according to the survey results, was 1.13% (780 out of 68989). However, the number of entered patients in the database was 501 (0.73%), but only 398 (0.58%) fulfilled the inclusion criteria. The mean age was 33.6± 14.3, 52% were female, 225 (56.5%) were CD, and 173 (46.4%) were UC. AP was clinically mild in most (86.9%) and, when imaging was performed (n=347, 86.7%), a normal pancreatic gland was described in 81 (23.3%), whereas edematous AP in 218 (62.8%). The most frequent etiology was the drug-induced (220, 55.3%), due to azathioprine in 172 (77.8%), with AP occurring at 2 mg/kg dosage, after a median duration of 1 month. Other causes included gallstones (59, 14.8%) and autoimmune (8.3%). In 54 (13.5%) AP was considered idiopathic. During a median follow-up of 67 months [IQR 34-96] from the index episode, 52 (13%) patients had AP recurrence, and 6 (1.5%) patients progressed to chronic pancreatitis. According to a subgroup analysis by IBD type, CD patients were more often smokers, had a family history of IBD and/or pancreatic disease, extraintestinal manifestations (arthropathy), and a history of surgery, usually ileocecal resection. Ileal location with or without colonic involvement was present in 90.3%, with non-stricturing non-penetrating behavior in most (56%). Medications (66.7%) and gallstones (17.8%) were CD's most common AP etiologies. In contrast, no risk factors for AP were found in UC patients, and extensive disease was described in 102 (59%). The etiology differed significantly from the CD group (p < 0.0001), since in addition to medication (40.5%), autoimmune pancreatitis was found in 13.9% and idiopathic AP in 22%.

	Overall N= 398	CD patients N= 225	UC patients N=173	P value
Sex Male Female	191 (48%) 207 (52%)	106 (47.1%) 119 (52.9%)	85 (49.1%) 88 (50.8%)	0.688
Mean age at AP onset (range)	37.6±15.3 (11-85)	39.2±14.9 (11-71)	35.5±15.6 (12-85)	0.970
EIMs No Yes	285 (71.6%) 113 (28.4%)	152 (67.5%) 73 (32.5%)	133 (76.9%) 40 (23.1)	0.040
Surgery for IBD Yes No	100 (25.1%) 298 (74.9%)	78 (34.6%) 147 (65.4%)	22 (12.7%) 151 (87.3%)	< 0.00001
Alcohol assumption at AP onset unknown none < 20 g/day >20 g/day binge drinking	59 (14.8%) 265 (66.6%) 57 (14.3%) 12 (3%) 5 (1.3%)	35 (15.6%) 146 (64.9%) 38 (16.9%) 4 (17.7%) 2 (0.9%)	24 (13.9%) 119 (68.8%) 19 (11%) 8 (4.6%) 3 (1.7%)	0.399
Smoking habit at AP onset unknown no smoker ex smoker median time from stop (years) active smoker mean cig/day (range)	14 (3.5%) 234 (58.8%) 44 (11%) 4.5 [1-9] 106 (26.7%) 13 (5-40)	8 (3.6%) 106 (47.1%) 24 (10.7%) 87 (38.6%)	6 (3.4%) 128 (74%) 20 (11.6%) 19 (11%)	< 0.00001
Pancreatic enzyme dosage unknown normal ≤2 fold unv ≥3 fold unv	24 (6%) 2 (0.5%) 30 (7.5%) 342 (86%)	12 (5.3%) 1 (0.4%) 16 (71.1%) 196 887.2%)	12 (6.9%) 1 (0.6) 14 (8.1%) 146 (95.4%)	0.439
Aetiology Idiopathic Drug-related Biliary Autoimmune Alcohol-related Dislipidemic/metabolic Post-endoscopic intervention# Others	54 (13.6%) 220 (55.3%) 59 (14.8%) 31 (7.8%) 14 (3.5%) 1 (0.2%) 4 (1%) 15 (3.8%)	16 (7.1%) 150 (66.7%) 40 (17.8%) 7 (3.1%) 4 (1.8%) 0 2 (0.9%) 6 (2.7%)	38 (21.9%) 70 (40.5%) 19 (11%) 24 (13.9%) 10 (5.8%) 1 (0.6%) 2 (1.2%) 9 (5.2%)	< 0.00001

Conclusion

PANDORA study established a 0.58% prevalence of AP in IBD patients, lower than expected. The AP is usually mild both clinically and radiologically. In 14% of cases no imaging is performed, in 23% pancreas is normal, suggesting that the real prevalence might be even lower. An ileal location in CD and extensive colitis in UC are usually reported and azathioprine seems the most common cause of AP in this setting, especially a few weeks after its introduction.

PREVALENCE, ETIOLOGY AND OUTCOME OF ACUTE PANCREATITIS IN INFLAMMATORY BOWEL DISEASE: EUROPEAN PANDORA STUDY

Maria Cristina Conti Bellocchi 1, Martina Cattani Mottes 2, Andreas Blesl 3, Anneline Cremer 4, Stefano Festa 5, Mathieu Uzzan 6, Tiago Cúrdia Gonçalves 7, Antonio Rispo 8, Chiara Vigano' 9, Ioannis Koutroubakis 10, Antonietta Gerarda Gravina 11, Daniela Pugliese 12, Piotr Eder 13, Sophie Vieujean 14, Massimo Claudio Fantini 15, Clara Yzet 16, Konstantinos Argyriou 17, Lieven Pouillon 18, Davide Giuseppe Ribaldone 19, Andrea Michielan 2, Natalia Swietek 20, Anna Viola 21, Edoardo Vincenzo Savarino 22, Pierre Ellul 23, María Chaparro 24, Spyridon Vrakas 25, Michele Campigotto 26, Raquel Oliveira 27, Angela Variola 28, Laura Loy 29, Alessia Dalila Guarino 8, Aldis Pukitis 30, Maria Fragaki 31, AIKATERINI MANTAKA 32, Laura Ramos Lopez 33, Rachele Ciccocioppo 1, Luca Frulloni 1

1 University of Verona, Verona, Italy

2 Santa Chiara Hospital, Trento, Italy

3 Medizinische Universität Graz, Graz, Austria

4 Erasme, Brussels, Belgium

5 San Filippo Neri Hospital, Rome, Italy

6 Hôpital Mondor, Paris, France

7 Hospital da Senhora da Oliveira - Guimarães, Guimarães, Portugal

8 University ´´Federico II´´of Naples, Naples, Italy

9 University of Milano-Bicocca School of Medicine, Monza, Italy

10 University Hospital Heraklion, Heraklion, Greece

11 University of Campania Luigi Vanvitelli, Naples, Italy

12 Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy

13 Heliodor Święcicki University Hospital, Poznań, Poland

14 CHU Liege Hospital, Liège, Belgium

15 University of Cagliari, Presidio Policlinico of Monserrato, Cagliari, Italy

16 Amiens univerisity hospital, Amiens, France

17 University Hospital Of Thessaly, Serres, Greece

18 Imelda Hospital Bonheiden, Bonheiden, Belgium

19 University of Turin, Turin, Italy

20 Universiteit Gent, Gent, Belgium

21 University of Messina, Messina, Italy

22 University of Padua, Division of Gastroenterology, Padua, Italy

23 Mater Dei Hospital, Msida, Malta

24 Hospital Universitario de La Princesa, Madrid, Spain

25 Tzaneio Hospital, Athens, Greece

26 Azienda Sanitaria Universitaria Giuliano Isontina, Trieste, Italy

27 Unidade Local de Saúde do Algarve - Portimão Unit, Cortegaça OVR, Portugal

28 IRCCS Ospedale Sacro Cuore Don Calabria Negrar, Negrar, Italy

29 Humanitas Clinical and Research Center, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rozzano, Italy

30 Pauls Stradins Clininic University Hopital Gastroenterology Center, Riga, Latvia

31 Venizeleion General Hospital, Heraklion, Greece

32 Chania General Hospital, Chania, Greece

33 Hospital Universitario de Canarias, Santa Cruz de Tenerife, Spain

Event

UEG Week Vienna 2024

Topics

Gut Microbiota IBD Pancreas

Submission format

Abstract

Session

What's new in acute pancreatitis

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Intestinal-failure-associated liver disease: What really matters?

Anna Simona Sasdelli 1

1 University of Bologna S. Orsola-Malpighi Hospital, Bologna, Italy

Event

UEG Postgraduate Teaching Programme Vienna 2024

Topics

Education & Training Hepatobiliary Primary Care

Session

Promoting rehabilitation and longevity in chronic intestinal failure

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Acute liver failure: How to rescue

Jonel Trebicka 1

1 Translational Hepatology - University Clinic Frankfurt, Frankfurt, Germany

Event

UEG Week Vienna 2024

Topics

Hepatobiliary Surgery

Session

Advances in metabolic disorders: Liver injury - prevent or rescue

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Psychology

Laurie Keefer 1

1 Icahn School of Medicine, New York, United States of America

Event

UEG Week Vienna 2024

Topics

Neurogastroenterology & Motility Primary Care

Session

The patient with a challenging functional disorder

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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