中文摘要：

目的通过观察热习服诱导的小鼠CD4^＋CD25^＋Foxp3^＋Treg细胞及中性粒细胞变化情况,探究热习服提高机体对高热环境耐受能力的机制。方法 6周龄C57BL/6小鼠常温（18~22℃）饲养30 d后进行43℃高热环境应激,观察150 min内小鼠存活率,并检测高热应激前后脾脏CD4^＋CD25^＋Foxp3^＋Treg细胞和中性粒细胞频率;同样6周龄C57BL/6小鼠在温度为34℃、湿度为65%的环境下进行饲养30 d,再进行43℃高热环境应激,观察150 min内小鼠生存率以及高热应激前后脾脏CD4^＋CD25^＋Foxp3^＋Treg细胞和中性粒细胞频率。通过对比,初步发现热习服后的小鼠存活率与脾脏的CD4^＋CD25^＋Foxp3^＋Treg细胞频率均有所上升;通过对比前后2组小鼠的脏器干湿质量比,判定发生肺水肿、实质脏器炎性渗出情况,明确热习服后的小鼠脏器损伤是否有所减轻,最后通过对2组小鼠脾脏CD4^＋CD25^＋Foxp3^＋Treg细胞和中性粒细胞的相关性进行分析,明确高热应激导致的小鼠脏器损伤、中性粒细胞在急性炎症初期的启动作用,以及Treg细胞对急性非特异性炎症的负调控之间的关联性。结果流式细胞术检测发现热习服组小鼠在高热处理前后,脾脏CD4^＋CD25^＋Foxp3^＋Treg细胞频率均普遍高于未热习服小鼠,而未热习服小鼠在高热应激后中性粒细胞的细胞频率表现出更加明显的上升,具有统计学差异（P〈0.05）;高热应激存活率对比发现热习服组小鼠在高热环境的生存率明显高于未热习服小鼠,而脏器炎性渗出及肺水肿程度更加轻微;相关性分析表明中性粒细胞与CD4^＋CD25^＋Foxp3^＋Treg细胞呈较为良好的负相关。结论热习服能够诱导机体分化产生更多的Treg细胞,从而更加有效地抑制高热应激下的炎症剧烈程度,对高热环境下机体的脏器起到保护作用。

英文摘要：

Heat acclimation is known to protect human body from heat related injure, and the physiological mechanisms inside were uncovered by lots of early studies. However, the immunological mechanisms of heat acclimation is not yet clear. CD4^＋CD25^＋Foxp3^＋Treg cells are known to suppress a wide range of immune responses through several different mechanisms. In our study, C57BL/6 mouse treated with a process of 30 d-heat acclimation were used to make sure whether the heat tolerance is related with the frequency of CD4^＋CD25^＋Foxp3^＋Treg cells in spleen, and methods used in this study contained survival-analysis, wet/dry weight ratio of organs, flow cytometry and correlation-analysis. Our result showed that after a process of 30 d-heat acclimation, the heat tolerance of C57BL/6 mouse enhanced; as the up-regulation of frequency of CD4^＋CD25^＋Foxp3^＋Treg cells in spleens, the frequency of neutrophil reduced, which was considered to be a protection factor to those mouse during heat stroke.We concluded that heat acclimation may induce the production of CD4^＋CD25^＋Foxp3^＋Treg cells to decrease the level of inflammation, and protect organs under heat stroke.