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Role of eosinophils in a murine model of inflammatory bowel disease
- Wang, Zi, Adachi, Soichiro, Kong, Lingling, Watanabe, Daisuke, Nakanishi, Yusuke, Ohteki, Toshiaki, Hoshi, Namiko, Kodama, Yuzo
- Biochemical and biophysical research communications 2019 v.511 no.1 pp. 99-104
- CCR3 receptor, T-lymphocytes, animal models, beta chemokines, colitis, colon, colonoscopy, enzyme-linked immunosorbent assay, eosinophils, histology, immunopathology, inflammation, interferon-gamma, interleukin-17, knockout mutants, lymph nodes, mice, patients, quantitative polymerase chain reaction
- Ulcerative colitis (UC) is a form of inflammatory bowel disease (IBD), which is triggered spontaneously by unknown mechanisms and manifests as chronic and relapsing inflammatory conditions in the colon. Eosinophil infiltration is often observed in the colonic tissue of ulcerative colitis patients. However, the role of eosinophils in the disease has not been well defined. The aim of this study is to investigate the role of eosinophils in colonic inflammation using the murine model of spontaneous colitis. CC chemokine receptor type 3 (CCR3) and interleukin (IL)-10 double knockout mice (CCR3−/−;IL-10−/−) were utilized to evaluate the function of eosinophils in colitis. The levels of colitis were evaluated by colonoscopy, histology, and real-time PCR measurements to determine expression levels of inflammatory cytokines in the colonic tissue. The levels of cytokines produced by T cells in mesenteric lymph nodes were evaluated by ELISA. There was no significant difference in endoscopic and histological scores between the groups of CCR3−/−;IL-10−/− mice and control CCR3+/−;IL-10−/− mice. There was also no significant difference in the expression levels of pro-inflammatory cytokines in the intestinal tissue between the two groups. Similar results were found for IL-17A and interferon gamma (IFN-γ) production from mesenteric lymph node-derived T cells. Our data indicate that eosinophils do not play a significant role in the immunopathology of colitis in IL-10−/− mice.