Imbalanced shift of cytokine expression between T helper 1 and T helper 2 (Th1/Th2) in intestinal mucosa of patients with post-infectious irritable bowel syndrome

Abstract

BackgroundIrritable bowel syndrome (IBS) is a common functional bowel disorder. The post-infectious IBS (PI-IBS) occurs in IBS patients with a history of intestinal infection preceding the onset of symptoms. However, the underlying cause of PI-IBS is not fully understood, and the purpose of this study was to investigate the immune regulatory mechanism of PI-IBS.MethodsParticipants enrolled in this study were divided into three groups including PI-IBS patients (n = 20), IBS patients without a history of infection (non-PI-IBS, n = 18), and healthy controls (n = 20). The expression levels of the Th1-derived cytokines IFN-γ and IL-12, and the Th2-derived cytokines IL-4 and IL-10 in the mucosal specimens, and in the ascending colon, the descending colon, and the rectal segments were measured by RT-PCR and western blot.ResultsThe IFN-γ mRNA levels in the intestinal mucosa were significantly higher in the PI-IBS group than in the non-PI-IBS or control group (both P < 0.05), but there was no difference between the non-PI-IBS and control groups. A trend toward IFN-γ protein upregulation was found in the PI-IBS group, while the IL-12 and IL-4 mRNA and protein levels were not different between any groups. The IL-10 mRNA and protein levels in the PI-IBS group were both significantly lower than in the non-PI-IBS or control groups (P < 0.05, respectively), but there was no difference between the non-PI-IBS and control groups. There were no differences in the cytokine mRNA and protein levels among the ascending colon, the descending colon, and the rectum of all groups.ConclusionsAn increase in IFN-γ levels and a decrease in IL-10 levels were found in the intestinal mucosa of PI-IBS patients, suggesting that the infection may affect the Th1/Th2 balance. Thus, the dysregulation of the immune response is likely an important cause of IBS.

Crosstalk at the mucosal border: importance of the gut microenvironment in IBS

“…184,185 Adaptive immunity Increased numbers of T cells within the epithelial layer, lamina propria or in the myenteric plexus of full-thickness or mucosal biopsy samples from the small and large intestine of patients with IBS have been reported in a number of publications. 141,[186][187][188][189] An immune response induced by type 1 T helper (T H 1) cells with increased IFN-γ and reduced IL-10 levels has been reported in postinfectious IBS, 190 whereas evidence of increased type 2 T helper (T H 2) cell activity has been reported in several functional gastrointestinal disorders. 177 The finding of normal frequencies of apparently functional blood and colonic CD25 + regulatory T cells, with the ability to suppress effector T-cell proliferation, 191 indicates that IBS is not associated with defective regulation of activated mucosal T cells.…”

Mast Cell-dependent Mesenteric Afferent Activation by Mucosal Supernatant From Different Bowel Segments of Guinea Pigs With Post-infectious Irritable Bowel Syndrome

“…A series of studies supported this immune dysfunction in IBS patients or animal models of IBS; for example, an imbalance between pro-inflammatory cytokines (TNF-, IL-1, IL-6, etc) and anti-inflammatory cytokines (IL-10, etc) with a Thl/Th2 shift in the gut was observed in PI-IBS. 33 The mucosal immune disorder was related to increased visceral pain. Cytokines such as IL-1 excited ENS neurons related to visceral hypersensitivity in IBS and inflammatory bowel disease.…”

Peroxiredoxin 1 as an inflammatory marker in diarrhea‐predominant and postinfectious irritable bowel syndrome

“…In all IBS patients, the serum PRDX1 (r = .335, P < .001) and TNF-α 16,33,[35][36][37] PRDX1 is associated with some tumors [21][22][23]38 and especially associated with colorectal cancer caused by chronic inflammation. 39,40 However, few studies have examined the relationship between PRDX1 and intestinal inflammation.…”