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Evidence for long-term sensitization of the bowel in patients with post-infectious-IBS.

Published version
Peer-reviewed

Type

Article

Change log

Authors

Balemans, D 
Mondelaers, SU 
Cibert-Goton, V 
Stakenborg, N 
Aguilera-Lizarraga, J 

Abstract

Post-infectious irritable bowel syndrome (PI-IBS) is a common gastrointestinal disorder characterized by persistent abdominal pain despite recovery from acute gastroenteritis. The underlying mechanisms are unclear, although long-term changes in neuronal function, and low grade inflammation of the bowel have been hypothesized. We investigated the presence and mechanism of neuronal sensitization in a unique cohort of individuals who developed PI-IBS following exposure to contaminated drinking water 7 years ago. We provide direct evidence of ongoing sensitization of neuronal signaling in the bowel of patients with PI-IBS. These changes occur in the absence of any detectable tissue inflammation, and instead appear to be driven by pro-nociceptive changes in the gut micro-environment. This is evidenced by the activation of murine colonic afferents, and sensitization responses to capsaicin in dorsal root ganglia (DRGs) following application of supernatants generated from tissue biopsy of patients with PI-IBS. We demonstrate that neuronal signaling within the bowel of PI-IBS patients is sensitized 2 years after the initial infection has resolved. This sensitization appears to be mediated by a persistent pro-nociceptive change in the gut micro-environment, that has the capacity to stimulate visceral afferents and facilitate neuronal TRPV1 signaling.

Description

Keywords

Adult, Animals, Capsaicin, Case-Control Studies, Colon, Cytokines, Female, Ganglia, Spinal, Gastroenteritis, Humans, Intestinal Mucosa, Irritable Bowel Syndrome, Male, Mice, Mice, Inbred C57BL, Middle Aged, Neurons, Receptors, Histamine H1, Signal Transduction, TRPV Cation Channels

Journal Title

Sci Rep

Conference Name

Journal ISSN

2045-2322
2045-2322

Volume Title

7

Publisher

Springer Science and Business Media LLC