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作 者:李红云[1] 姚咏明[1] 姚凤华[1] 董宁[1] 于燕[1] 施志国 盛志勇[1]
机构地区:[1]解放军总医院第三O四临床部全军烧伤研究所基础部,北京100037
出 处:《中华创伤杂志》2004年第12期734-738,共5页Chinese Journal of Trauma
基 金:国家重点基础研究发展规划基金资助项目(G19990 5 42 0 3 );国家杰出青年基金资助项目 (3 0 12 5 0 2 0 );首都医学发展科研基金重点资助项目 (2 0 0 3 -2 0 15 )
摘 要:目的 观察烫伤后金黄色葡萄球菌 (金葡菌 )脓毒症大鼠重要脏器细胞因子信号转导抑制因子 (SOCSs)基因表达的规律及其与细胞因子变化的关系。 方法 采用大鼠 2 0 %体表面积Ⅲ度烫伤后金葡菌攻击致脓毒症模型 ,检测动物肝、肺组织中SOCS1、SOCS2和SOCS3mRNA表达 ,并测定组织中干扰素 -γ(IFN -γ)水平。 结果 烫伤后金葡菌感染大鼠肝、肺组织IFN -γ产生均显著增多 ,分别于伤后 0 .5和 6h达峰值 (P <0 .0 1 )。同时 ,动物肺组织SOCS1、SOCS2和SOCS3mRNA表达均明显上调 ,其中SOCS2和SOCS3mRNA表达改变较为迅速 ,伤后 0 .5h即明显高于对照组 ,2h达峰值。肝组织SOCS1mRNA表达于伤后 2h明显增强 ,2 4h仍维持于较高水平 ;而肝脏SOCS2和SOCS3mRNA表达仅呈现升高趋势。金葡菌肠毒素B单克隆抗体早期干预后 ,随着肺脏IFN -γ产生减少 ,肺组织SOCS1、SOCS2和SOCS3基因表达亦明显降低。 结论 烫伤后金葡菌感染可诱导体内SOCSs表达上调 ,其改变与IFN -γ的“消涨”密切相关 ,提示它们可能参与了金葡菌脓毒症时炎症反应平衡的调节过程。Objective To observe the expression law of cytokine signaling suppressors (SOCSs) mRNA in burn rats with Staphylococcus aureus sepsis and investigate their potential role in the pathogenesis of postburn sepsis. Methods Wistar rats were inflicted with 20% TBSA Ⅲ° scald, followed by Staphylococcus aureus challenge. Then, the expressions of SOCS1, SOCS2 and SOCS3 mRNA and interferon-γ (IFN-γ) levels in the liver and lungs were determined. Results With Staphylococcus aureus challenge after burn, IFN-γ levels in the liver and lungs were significantly elevated and reached peak at the 0.5th and 6th hours, respectively (P<0.01). Meanwhile, after Staphylococcus aureus challenge, in the lungs a rapid up-regulation was found upon the expressions of SOCS mRNA, especially SOCS2 and SOCS3 mRNA, in which the expressions were obviously higher than those in the controls at the 0.5th hour and reached peak at the 2nd hour. In contrast, SOCS1 gene expression in the liver was markedly increased at the 2nd hour, remaining high up to 24 hours. However, the expressions of SOCS2 and SOCS3 only showed a trend of up-regulation in the liver. Early treatment with monoclonal antibody to Staphylococcal enterotoxin B could effectively inhibit the expressions of pulmonary IFN-γ production, SOCS1 and SOCS2 in the lungs in accordance with reduction of pulmonary IFN-γ production. Conclusions Burn injury combined with Staphylococcus aureus challenge can induce the upregulation of the gene expressions of SOCSs, which closely correlates to the changes of IFN-γ, indicating that IFN-γ may participate in regulating the balance of inflammatory response in posturn Staphylococcus aureus sepsis.
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