Th17 cells influence intestinal muscle contraction during Trichinella spiralis infection

Abstract

Trichinella spiralis infection in rodents is a well-known model of intestinal inflammation associated with hypermotility. The aim of the study was to use this experimental model to elucidate if Th17 cells are involved in the development of gastrointestinal hypermotility. Colonic smooth muscle contractility was investigated in response to acetylcholine. The levels of IL-17, IL-23 and TGF-beta1 in colon were measured by Western blotting. Flow cytometric detection of intracellular IFN-gamma/IL-4/IL-17 cytokine production was used to analyze the proportions of CD4+ T cells subsets in colon. Our results showed that colonic muscle contractility was increased 2 weeks post infection (PI) and stayed high 12 weeks PI when no discernible inflammation was present in the gut. The proportion of Th17 cells and the expression of IL-17 were up-regulated in colon 2 weeks PI and returned to normal 8 weeks PI. The content of IL-17 was correlated with the colonic smooth muscle hypercontracility 2 weeks PI. Meanwhile, TGF-beta1 was increased 2 weeks PI, while IL-23 was normal. Our results suggest that Th17 cells affect the colonic muscle contractility in mice infected with Trichinella spiralis at intestine stage but not at muscle stage and the effect of Th17 cells on muscle contractility might be induced by TGF-beta1. Other cytokines might be involved in the hypercontracility of colonic smooth muscle at muscle stage.

IL-17A promotes protective IgA responses and expression of other potential effectors against the lumen-dwelling enteric parasite Giardia

“…Although the underlying effector mechanisms are not known, IL-17A was not important for controlling intestinal NOS expression, which can contribute to antigiardial defense (Tako, et al, 2013), or for mediating intestinal hypermotility, a key effector of antigiardial immune defense (Andersen, et al, 2006; Li, et al, 2006). This is in contrast to the findings with another lumen-dwelling parasite, the nematode Trichinella spiralis , where IL-17A promotes hypermotility during infection (Fu, et al, 2009), underlining that the actions of IL-17A can be mediated by different immune effectors.…”

Transfer of CD11c+ lamina propria mononuclear phagocytes from post-infectious irritable bowel syndrome causes mucosal barrier dysfunction and visceral hypersensitivity in recipient mice

“…The major characteristics of IBS include visceral hypersensitivity, altered secretion, intestinal sensory nerve abnormalities, barrier dysfunction and alterations in intestinal immune function. Consequently, mouse models of PI-IBS based on T. spiralis infection are widely used to investigate both the immunological and functional changes associated with gut inflammation, as described in previous studies (45,46).…”

A review of the irritable bowel syndrome investigation on epidemiology, pathogenesis and pathophysiology in China

“…reported a delayed gastric emptying in C‐IBS patients and increased gastric emptying in D‐IBS patients. Further study found that the proximal stomach accommodation in both C‐IBS and D‐IBS, which suggested that the accelerated gastric emptying in D‐IBS maybe partly contributed to the impaired stomach accommodation but not C‐IBS 29 . Although the abnormal gastrointestinal motility is widely reported in IBS, the relationship between the dysmotility and symptoms is inconsistent.…”

“…investigated the shift of Th1/ Th2 / Th17 balance in colon mucosa, which showed enhanced Th17 activity, but there was no any change in the peripheral blood lymphocytes, in a post Trichinella spiralis infection model. The hypercontractility of colonic muscle was mediated by Th17 cells/TGFβ1 in acute phase and IL‐17 in chronic phase in the post‐infection model 29 . Linghu et al .…”