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Title: Characteristics of intestinal lamina propria dendritic cells in a mouse model of postinfectious irritable bowel syndrome. Author: Long Y, Wang W, Wang H, Hao L, Qian W, Hou X. Journal: J Gastroenterol Hepatol; 2012 May; 27(5):935-44. PubMed ID: 22141367. Abstract: 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.[Abstract] [Full Text] [Related] [New Search]