- 作者：Masahito Ogiku ; M.D. ; Hiroshi Kono ; Ph.D. ; hkouno@yamanashi.ac.jp ; Michio Hara ; M.D. ; Masato Tsuchiya ; Ph.D. ; Hideki Fujii ; Ph.D.
- 关键词：interleukin-17A ; interleukin-17A knockout mouse ; sepsis ; high mobility group box 1 ; regulatory T cell
- 刊名：Journal of Surgical Research
- 出版年：2012
- 期刊代码：299_00224804
- 类别：med
- 出版时间：1 May, 2012
- 卷：174
- 期：1
- 页码：142-149
- 文件大小：1842 K
Background
Interleukin (IL)-17A is a proinflammatory cytokine and plays an important role in neutrophil recruitment. We investigate the role of IL-17A in a mouse polymicrobial sepsis model.Materials and Methods
IL-17A knockout mice (KO) and wild-type (WT) mice were subjected the cecal ligation and puncture (CLP). Survival was assessed for the following 7 d after the CLP operation, and histopathologic findings were evaluated 12 h after CLP. Bacterial outgrowth in blood was assessed by blood culture 12 h after CLP. After CLP, expression of inflammatory mediators in serum was assessed by enzyme-linked immunosorbent assay (ELISA). Furthermore, expression of FOXP3 and IL-17A in the spleen was assessed by immunohistochemical staining and flow cytometry.
Results
Mortality was increased in KO mice compared with WT mice after CLP. Furthermore, bacterial outgrowth in blood and serum high mobility group box 1 (HMGB1) levels were also significantly greater in KO mice than WT mice. The expression of FOXP3 in the spleen was significantly greater in KO mice than WT mice.
Conclusion
IL-17A play pivotal role in host defense during septic peritonitis.