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Psychological comorbidity increases the risk for postinfectious IBS partly by enhanced susceptibility to develop infectious gastroenteritis
  1. Mira M Wouters1,
  2. Sander Van Wanrooy1,
  3. Anh Nguyen2,3,
  4. James Dooley2,3,
  5. Javier Aguilera-Lizarraga1,
  6. Winde Van Brabant1,
  7. Josselyn E Garcia-Perez2,3,
  8. Lukas Van Oudenhove1,
  9. Marc Van Ranst4,
  10. Jan Verhaegen5,
  11. Adrian Liston2,3,
  12. Guy Boeckxstaens1
  1. 1Department of Clinical and Experimental Medicine, Translational Research Center for Gastrointestinal Disorders, University Hospital Leuven, KU Leuven, Leuven, Belgium
  2. 2Department of Microbiology and Immunology, KU Leuven, Leuven, Belgium
  3. 3Autoimmune Genetics Laboratory, VIB, Leuven, Belgium
  4. 4Laboratory of Clinical Virology, Rega Institute for Medical Research, University Hospital Leuven, Leuven, Belgium
  5. 5Department of Microbiology, University Hospital Leuven, KU Leuven, Leuven, Belgium
  1. Correspondence to Professor Guy Boeckxstaens Translational Research Center for Gastrointestinal Disorders (TARGID), Center of Neuroimmune interaction and Mucosal Immunology, KU Leuven, University Hospital of Leuven, Herestraat 49, Leuven 3000, Belgium; guy.boeckxstaens{at}med.kuleuven.be

Abstract

Objective Psychological factors increase the risk to develop postinfectious IBS (PI-IBS), but the mechanisms involved are unclear. As stress affects the immune system, we investigated the potential interaction between psychological factors, the immune response against infectious gastroenteritis (IGE) and the development of IGE and PI-IBS in a large cohort exposed to contaminated drinking water.

Design 18 620 people exposed to contaminated drinking water (norovirus, Giardia lamblia, Campylobacter jejuni) were invited to participate in a prospective controlled cohort study. They were asked to complete questionnaires assessing demographic, psychological and clinical data during the outbreak and 1 year later. At both time points, in-depth immune function (peripheral blood and rectal biopsies) was studied in a subgroup of subjects.

Results 1379 subjects completed the questionnaires during the outbreak, of which 271 developed IGE. Risk factors for IGE included younger age, pre-existing dyspepsia-like symptoms, anxiety and drinking contaminated tap water. Anxiety scores before the outbreak inversely correlated with interleukin-2-expressing CD4+ T cells (r=0.6, p=0.01, n=23). At follow-up, 34 of 172 (20%) IGE subjects developed IBS compared with 24/366 exposed participants (7%, p<0.0001, χ2 test). A Th2 cytokine phenotype at time of infection was associated with increased risk for PI-IBS 1 year later. Except for increased B cell numbers, no evidence for systemic or rectal mucosal immune activation in PI-IBS was demonstrated at follow-up.

Conclusions Our study shows that the increased risk of patients with psychological comorbidity to develop PI-IBS may partly result from an increased susceptibility to develop IGE, possibly resulting from a Th2-immune bias.

Trial registration number (ClinicalTrials.gov NCT01497847).

  • IGE
  • IRRITABLE BOWEL SYNDROME

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