Acute psychological stress increases small intestinal permeability in humans. Peripheral CRH reproduces the effect of stress and DSCG blocks the effect of both stress and CRH, suggesting the involvement of mast cells. These findings provide new insight into the complex interplay between the central nervous system and GI function in man.

In studies of rectal biopsy specimens from patients, we found that HRH1-mediated sensitization of TRPV1 is involved in IBS. Ebastine, an antagonist of HRH1, reduced visceral hypersensitivity, symptoms, and abdominal pain in patients with IBS. Inhibitors of this pathway might be developed as a new treatment approach for IBS. ClinicalTrials.gov no: NCT01144832.

(ClinicalTrials.gov NCT01497847).

Rs2349775 (NXPH1) and rs17837965 (CDC42) were associated with IBS-D and IBS-C, respectively, in two independent cohorts. Further studies are warranted to validate our findings and to determine the mechanisms underlying IBS pathophysiology.

WA stress induced increased pain perception as well as activation of the somatosensory cortex, PAG, and hippocampus in maternal-separated rats. These findings are in line with human studies and provide indirect evidence that the maternal separation model mimics the cerebral response to visceral hypersensitivity in humans.

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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.

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