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Background: Mucosal immune activation has been postulated to play an important role in the pathogenesis of irritable bowel syndrome (IBS). However, data are conflicting and often based on small patient cohorts. Here, we aimed to evaluate the gene expression of a large set of immune‐related genes in mucosal biopsies from IBS patients and healthy volunteers (HV). Methods: A total of 171 IBS patients and 127 HV were included in the study. Rectum biopsies were collected from a cohort of 70 HV and 77 IBS patients (Rome III) and colon descendens biopsies from another cohort of 57 HV and 94 IBS patients (Rome II). Gene expression was assessed using OpenArray technology, and validated questionnaires were used to evaluate clinical characteristics (GI symptoms, somatization, anxiety, and depression). Key Results: A subset of IBS patients (33%) with increased immune activation in the colon descendens was identified using multivariate analysis and displayed increased gene expression of IL1B (3‐fold change), prostaglandin synthase PTGS2 (2.1‐fold change), and the G‐protein‐coupled receptor MRGPRX2 (10.7‐fold change). Clinical characteristics in this subgroup were however similar to the rest of the patient cohort. Analysis of rectal biopsies failed to identify such subgroup of "immuno‐active" IBS patients in the other patient cohort. Conclusion: A subset of IBS patients reveals evidence of immune activation in the colon descendens, but not in the rectum; however, gene expression is unrelated to clinical symptoms. To what extent this subgroup might however respond to anti‐inflammatory therapy remains to be investigated. [ABSTRACT FROM AUTHOR]

Background: The role of persistent immune activation in postinfectious irritable bowel syndrome (PI‐IBS) remains controversial. Here, we prospectively studied healthy subjects traveling to destinations with a high‐risk to develop infectious gastroenteritis (IGE) in order to identify immune‐mediated mechanisms and risk factors of PI‐IBS. Methods: One hundred and one travelers were asked to complete questionnaires on psychological profile and gastrointestinal (GI) symptoms before travel, 2 weeks, 6 months and 1 year after travel. At each visit, blood was collected for PBMC isolation and rectal biopsies were taken. PI‐IBS was diagnosed using the Rome III criteria and subjects with persistent postinfectious abdominal complaints (PI‐AC) were identified using 3 GSRS symptoms (ie, loose stools, urgency and abdominal pain). Results: Forty‐seven of the 101 subjects reported IGE during travel. After 1 year, two subjects were diagnosed with PI‐IBS and eight subjects were presented with PI‐AC versus two subjects with IBS and two with abdominal complaints in the non‐infected group. PBMC analysis showed no differences in T and B cell populations in subjects with PI‐AC vs healthy. Additionally, no differences in gene expression were observed in the early postinfectious phase or after 1 year. Regression analysis identified looser stools, higher anxiety and somatization before infection and several postinfectious GI symptoms as risk factors for PI‐AC. Conclusions: The incidence of PI‐IBS is low following travelers' diarrhea and there is need for larger studies investigating the role of immune activation in PI‐IBS. Psychological factors before infection and the severity of symptoms shortly after infection are risk factors for the persistence of PI‐AC. In this study, we prospectively studied healthy subjects traveling to destinations with a high risk to develop infectious gastroenteritis in order to identify immune‐mediated mechanisms and risk factors of PI‐IBS. We demonstrated that the incidence of PI‐IBS is low after TD compared to outbreak studies. As the number of patients who developed PI‐IBS or persistent abdominal complaints was low, no firm conclusions could be drawn with respect to the role of immune activation. Nonetheless, our study confirms the importance of psychological factors prior to infection and the severity of abdominal symptoms in the early post‐infectious period as risk factors for persistent post‐infectious abdominal complaints. [ABSTRACT FROM AUTHOR]