结肠炎
粒细胞巨噬细胞集落刺激因子
细胞因子
免疫学
生物
炎症性肠病
炎症
发病机制
免疫系统
单核细胞
肿瘤坏死因子α
内科学
医学
疾病
作者
Yinghua Xu,Nicholas H. Hunt,Shisan Bao
出处
期刊:Cell Research
[Springer Nature]
日期:2008-12-01
卷期号:18 (12): 1220-1229
被引量:89
摘要
An imbalance of mucosal pro- and anti-inflammatory cytokines is crucial in the pathogenesis of inflammatory bowel disease (IBD). GM-CSF influences the development of hemopoietic cells. The precise role of GM-CSF in IBD remains to be elucidated. GM-CSF gene knockout (GM-CSF−/−) and wild-type (Wt) mice were challenged with 2.5% dextran sulfate sodium (DSS) for 7 days. The ensued clinical and pathological changes, macrophage infiltration, colonic cytokine production, and bacterial counts were examined. DSS-treated GM-CSF−/− mice developed more severe acute colitis than DSS-treated Wt mice, reflected by a greater body weight loss, more rectal bleeding, and aggravated histopathological changes. More infiltrating macrophages were observed in GM-CSF−/−, compared with Wt mice following DSS challenge, correlating with monocyte chemoattractant protein-1 (MCP-1) production. The levels of colonic IL-17 and TNF-α were increased significantly in GM-CSF−/− mice, but not in Wt mice, following DSS administration. The level of IL-6 was increased by 1.5- and 2-fold in the colon of GM-CSF−/− and Wt mice, respectively, following DSS challenge. No significant changes in IL-4 and IFN-γ were detected in Wt and GM-CSF−/− mice following DSS treatment. The bacteria recovery from colon was increased about 15- and 5-fold, respectively, in Wt mice and GM-CSF−/− mice following DSS challenge. These results suggest that GM-CSF−/− mice are more susceptible to acute DSS-induced colitis, possibly because of an impaired gut innate immune response as a result of diminished GM-CSF.
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