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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。
Objective To observe the changes of CD4 + CD25 + Foxp3 + Treg cells and neutrophils in mice induced by heat acclimatization and explore the mechanism of heat acclimatization to improve the tolerance of the body to hyperthermia. Methods C57BL / 6 mice at 6 weeks old were housed for 30 days at normal temperature (18-22 ℃) and then exposed to hyperthermia at 43 ℃. The survival rate of mice was observed after 150 min. The levels of CD4 + CD25 + Foxp3 + Treg cells and neutrophil frequency. Similarly, 6-week-old C57BL / 6 mice were housed for 30 days at 34 ℃ and 65% humidity, and then exposed to hyperthermia at 43 ℃ for 150 min Survival rate of mice and the spleen CD4 + CD25 + Foxp3 + Treg cells and neutrophil frequency before and after high heat stress. By comparison, we found that the survival rate of mice after heat acclimation and the spleen CD4 + CD25 + Foxp3 + Treg cells were increased; by comparing the two groups before and after the organ of the wet and dry weight ratio of organs to determine the occurrence of pulmonary edema , The essence of inflammatory exudative organs, a clear heat organ damage after organ damage have been reduced, and finally by the two groups of mice spleen CD4 + CD25 + Foxp3 + Treg cells and neutrophils correlation Analysis of the high heat stress induced organ damage in mice, the initial role of neutrophils in acute inflammation, as well as Treg cells associated with acute non-specific inflammation negative regulation. Results The results of flow cytometry showed that the frequencies of CD4 + CD25 + Foxp3 + Treg cells in the heat-treated mice were significantly higher than those in the non-heat-fed mice before and after heat-treatment, Post-neutrophil cell frequency showed a more significant increase, with a statistically significant difference (P <0.05); high heat-stress survival comparison found that heat-fed mice in high-heat environment survival rate was significantly higher than the non-heat-Xi Mice, and organ inflammatory exudation and pulmonary edema degree is more minor; correlation analysis showed that neutrophils and CD4 + CD25 + Foxp3 + Treg cells showed a relatively good negative correlation. Conclusion Heat acclimation can induce the differentiation of the body to produce more Treg cells, which can more effectively inhibit the severity of inflammation under high heat stress and play a protective role on the organs of the organism under high heat environment.