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.
Highlights
Irritable bowel syndrome (IBS) is a common functional bowel disorder
Cytokine mRNA levels in the intestinal mucosa The results of RT-PCR assays showed that IFN-γ levels were significantly higher in the intestinal mucosa of PIIBS patients (0.47 ± 0.02) than that in non-post-infectious IBS (PI-IBS) patients (0.32 ± 0.02) or healthy people (0.31 ± 0.02), but there was no significant difference between the non-PI-IBS and control groups (P > 0.05)
For IL-12 and IL-4 levels in the intestinal mucosa, no significant differences were noted in PI-IBS patients (0.24 ± 0.01 for IL-12 and 0.33 ± 0.02 for IL-4) compared to non-PI-IBS patients (0.22 ± 0.01 for IL-12 and 0.31 ± 0.02 for IL-4) or healthy people (0.22 ± 0.02 for IL12 and 0.33 ± 0.02 for IL-4), or between the non-PI-IBS and control groups (P > 0.05)
Summary
Irritable 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. Irritable bowel syndrome (IBS) is a common intestinal disorder characterized by persistent or intermittent abdominal pain or discomfort, distention, and changes in stool patterns. Th1 cells predominantly secrete IFN-γ, IL-12, IL-2, and tumor necrosis factor-α (TNF-α), and mediate cellular immunity, while Th2 cells play a key role in promoting Th1 differentiation and the Th1 response. Studies confirm that Th1 and Th2 cells function as a pair of important regulators that restrain one another and produce cytokines, which interact to maintain a balanced immune response [4]. It has been confirmed that patients with both inflammatory bowel disease (IBD) and Th1/Th2 disequilibrium often develop IBS symptoms [6], which suggests that PI-IBS may result from abnormal Th1/Th2 immune regulation. We chose the four main cytokines, IFN-γ, IL-12, IL-4 and IL-10, to observe the changes in Th1- and Th2-derived cytokines in the intestinal mucosa and to explore the Th1/Th2 shift and its potential role in PI-IBS patients
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