摘要: |
目的:探讨信号转导及转录激活蛋白4(signal transducer and activator of transcription 4, STAT4)在细菌表面分子脂多糖(LPS)所致急性肺损伤(ALI)中的作用及可能机制。方法:建立STAT4基因敲除小鼠模型,采用LPS诱导小鼠肺损伤并观察肺组织病理变化及血气分析变化,流式细胞仪分析外周血骨髓源性抑制细胞(MDSC)和调节性CD4+CD25+Treg细胞的变化情况,瑞氏染色观察肺部炎症细胞浸润情况。结果:在LPS诱导的肺损伤模型中,STAT4基因敲除小鼠肺组织损害较野生型小鼠肺损伤减轻,动脉血氧合指数(PaO2/FiO2)高,病理评分降低,肺湿/干重比降低,外周血MDSC和CD4+CD25+Treg升高,肺部炎性细胞总数增加,中性粒细胞浸润增加(P<0.05)。结论:STAT4可加重LPS诱导的肺损伤,可能与MDSC及CD4+CD25+Treg细胞在外周血的比例升高有关。 |
关键词: 信号转导及转录激活蛋白4 脂多糖 肺损伤 |
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Abstract: |
To discuss the effect of signal transducer and activator of transcription 4 (STAT4) in bacteria lipopolysaccharide (LPS) induced acute lung injury (ALI) on mice. Methods:Mice with gene STAT4 knocked out (STAT4-/-) were used. In the models of LPS induced ALI model, arterial blood gas analysis was utilized, and change of myeloid derived suppressor cells (MDSCs) and regulator CD4+CD25+Treg cells were observed using flow cytometry. Pulmonary inflammatory cells were analyzed by Wright stain.Results:In the models of LPS induced ALI, lung injury was alleviated in STAT4-/- mice compared to wild type (WT) mice. PaO2/FiO2 was higher, histological score was lower, lung wet/dry ratio decreased, MDSCs and CD4+CD25+Treg cells were increased, total number of inflammatory cells and neutrophils were higher in STAT4-/- mice compared to WT mice (P<0.05). Conclusions:Deficiency of STAT4 could alleviate LPS induced ALI. The potential mechanism may be associated with increased ratios of MDSCs and CD4+CD25+Treg cells in the blood. |
Key words: signal transducer and activator of transcription 4 lipopolysaccharide lung injury |