Effects of heat stroke on CD4+CD25+Foxp3+ regulatory T cells in rats / 解放军医学杂志

ABSTRACT

Objective To better understand the immune status in the rats after heatstroke. Methods Adult male SD rats were randomized into 3 groups control group (n=20), classic heatstroke group (CHS, n=60) and exertional heatstroke group (EHS, n=60). Flow cytometry was employed to detect the percentage of CD4+CD25+Foxp3+ regulatory T cells (Tregs) in arterial blood and spleen as well as the apoptosis rate of Tregs in the spleen. To trace the dynamic changes on Treg cells, samples were collected at specific time points after heatstroke modeling (0, 6, 12, 24, 48, 72 hours post heatstroke). Results The proportion of Tregs in artery blood and spleen in CHS group increased gradually with a percentage lower than those in control group at first 24 h but higher than those in control group after 24 h. Interestingly, the proportion of Tregs in artery blood and spleen in EHS group was gradually reduced over time. The Tregs in the artery blood slightly higher than that in control group at 0 h followed by less than that in control group afterward; while Tregs in the spleen were higher than that in control group within 12 h, followed by less than that in control group after 24 h. The proportion of apoptotic Tregs in the spleen in CHS group was gradual decline over time, in the first 12 h they were higher than that in control group but lower than that in control group after 24 h. On the contrary, the proportion of apoptotic Tregs in the spleen in EHS group was gradually increased over time and was higher than that in control group at all time points. Conclusions The proportion of Tregs in peripheral blood and spleen in CHS group showed a rising trend during the early period. This is consistent with the trend in the spleen Tregs apoptosis rate, indicated that immunosuppression may have appeared in the early onset of CHS rats. However, the proportion of Tregs in peripheral blood and spleen in EHS group showed a trend of gradual reduction which is consistent with the spleen Tregs apoptosis rate. The opposite phenotype detected from CHS and EHS rats may due to the excessive inflammatory reaction promoted the apoptosis of Tregs in EHS rats.