Background and aim: Postinfectious irritable bowel syndrome (PI-IBS), which results from inflammation has been emphasized a lot recently. Dendritic cells (DCs) may contribute to intestinal mucosal immune activation in the pathogenesis of PI-IBS. This study tested the hypothesis that phenotype and function of intestinal lamina propria DCs (LPDCs) changed in the development of a PI-IBS mouse model.
Methods: Mice infected with Trichinella spiralis underwent abdominal withdrawal reflex (AWR) to evaluate visceral sensitivity. LPDCs were isolated and purified by intestine digestion and magnetic label-based technique. Surface markers were analyzed by flow cytometry. Endocytic activity, mixed lymphocyte reaction (MLR) and chemotaxis were studied. Cytokine production of the LPDCs cocultured with CD4(+) T cells was determined.
Results: Intestinal inflammation resolved after 8 weeks infection with sustained visceral hyperalgesia. Surface markers CD86 and MHCII were lower in the acute infection group, but increased in the PI-IBS stage. Enhanced ability of endocytic activity and decreased abilities to attract and stimulate CD4(+) T cell proliferation were in the acute infection group. However, LPDCs in the PI-IBS stage showed weakened endocytic ability with enhanced abilities to attract and stimulate CD4(+) T cell proliferation. Cocultured LPDCs with CD4(+) T cells showed a predominant Th2 response in the acute infection stage, and more important roles of Th1, Th17 responses in the PI-IBS stage.
Conclusions: The hypothesis was supported that the phenotype and function of LPDCs changed in the development of PI-IBS, which induced the maintenance of intestinal mucosal immune activation and might provide a clue for the treatment of the disease.
© 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd.