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Role of interleukin 18 in acute lung inflammation induced by gut ischemia repeifusion
作者姓名:Yong-Jie Yang  Institute of Biochemistry and Cell Biology  Shanghai Institutes for Biological Sciences  Chinese Academy of Sciences  Graduate School of the Chinese Academy of Sciences  Shanghai  China Yun Shen  
作者单位:Yong-Jie Yang,Institute of Biochemistry and Cell Biology,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences; Graduate School of the Chinese Academy of Sciences,Shanghai 200031,China Yun Shen,Department of Traditional Chinese Medicine,Shanghai University of Traditional Chinese Medicine,Shanghai 201023,China Song-Hua Chen,Xi-Rui Ge,Institute of Biochemistry and Cell Biology,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences,Shanghai 200031,China
基金项目:Supported by the CAS Pilot Project of Knowledge Innovation Program, No. KSCX 2-3-04-03
摘    要:AIM: To study the changes of endogenous interleukin 18 (IL-18) levels and evaluate the role of IL-18 on lung injury following gut ischemia/reperfusion. METHODS: A superior mesenteric artery occlusion model was selected for this research. The mice were randomly divided into four groups: Sham operation (sham), ischemia (0.5 h) followed by different times of reperfusion (I/R), and I/R pretreated with exogenous IL-18 (I/R+IL-18) or IL-18 neutralizing antibody (I/R+IL-18Ab) 15 min before ischemia. Serum IL-18 levels were detected by Western blot and ELISA, and the levels of IL-18 in lung tissue were evaluated by immunohistochemical staining. For the study of pulmonary inflammation, the lung myeloperoxidase (MPO) contents and morphological changes were evaluated. RESULTS: Gut ischemia/reperfusion induced rapid increase of serum IL-18 levels, peaked at 1 h after reperfusion and then declined. The levels of IL-18 in lung tissue were gradually enhanced as the progress of reperfusion. Compared with I/R group, exogenous administration of IL-18 (I/R+IL-18) further remarkably enhanced the pulmonary MPO activity and inflammatory cell infiltration, and in I/R+IL-18Ab group, the content of MPO were significantly reduced and lung inflammation was also decreased. CONCLUSION: Gut ischemia/reperfusion induces the increase of IL-18 expression, which may make IL-18 act as an important proinfiammatory cytokine and contribute to gut ischemia/reperfusion-induced lung inflammation.


Role of interleukin 18 in acute lung inflammation induced by gut ischemia repeifusion
Yong-Jie Yang,Institute of Biochemistry and Cell Biology,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences,Shanghai ,China Yun Shen,.Role of interleukin 18 in acute lung inflammation induced by gut ischemia repeifusion[J].World Journal of Gastroenterology,2005(29).
Authors:Yong-Jie Yang
Institution:Yong-Jie Yang,Institute of Biochemistry and Cell Biology,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences,Shanghai 200031,China Yun Shen,Department of Traditional Chinese Medicine,Shanghai University of Traditional Chinese Medicine,Shanghai 201023,China Song-Hua Chen,Xi-Rui Ge,Institute of Biochemistry and Cell Biology,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences,Shanghai 200031,China
Abstract:AIM: To study the changes of endogenous interleukin 18 (IL-18) levels and evaluate the role of IL-18 on lung injury following gut ischemia/reperfusion. METHODS: A superior mesenteric artery occlusion model was selected for this research. The mice were randomly divided into four groups: Sham operation (sham), ischemia (0.5 h) followed by different times of reperfusion (I/R), and I/R pretreated with exogenous IL-18 (I/R+IL-18) or IL-18 neutralizing antibody (I/R+IL-18Ab) 15 min before ischemia. Serum IL-18 levels were detected by Western blot and ELISA, and the levels of IL-18 in lung tissue were evaluated by immunohistochemical staining. For the study of pulmonary inflammation, the lung myeloperoxidase (MPO) contents and morphological changes were evaluated. RESULTS: Gut ischemia/reperfusion induced rapid increase of serum IL-18 levels, peaked at 1 h after reperfusion and then declined. The levels of IL-18 in lung tissue were gradually enhanced as the progress of reperfusion. Compared with I/R group, exogenous administration of IL-18 (I/R+IL-18) further remarkably enhanced the pulmonary MPO activity and inflammatory cell infiltration, and in I/R+IL-18Ab group, the content of MPO were significantly reduced and lung inflammation was also decreased. CONCLUSION: Gut ischemia/reperfusion induces the increase of IL-18 expression, which may make IL-18 act as an important proinfiammatory cytokine and contribute to gut ischemia/reperfusion-induced lung inflammation.
Keywords:IL-18  Ischemia  Reperfusion Inflammation
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