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(PaO_2/FiO_2)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。
Objective：To discuss the effect of signal transducer and activator of transcription 4（STAT4） in bacterialipopolysaccharide（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 STAT 4-/-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 STAT 4-/-mice compared to WT mice（P〈0.05）.Conclusions：Deficiency of STAT 4 could alleviate LPS induced ALI.The potential mechanism may be associated with increased ratios of MDSCs and CD4^＋CD25^＋Treg cells in the blood.
出处
《中国临床医学》
2017年第4期519-524,共6页
Chinese Journal of Clinical Medicine
基金
国家自然科学基金(81500058)
上海市卫生和计划生育委员会课题(15GWZK0102)
上海市公共卫生三年行动计划重点学科建设项目传染病与卫生微生物学(2016/01-2017/12)
福建省自然科学基金面上项目(2017J01140)~~
关键词
信号转导及转录激活蛋白4
脂多糖
肺损伤
signal transducer and activator of transcription 4
lipopolysaccharide
lung injury
