Effect of acute heat stress on calcium concentration, proliferation, cell cycle, and interleukin-2 production in splenic lymphocytes from broiler chickens.

In the present study, we investigated the effects of acute heat stress on the concentration of free Ca2+ ([Ca2+]i) and markers of cellular immunity in splenic lymphocytes from broiler chickens. Eighty 6-wk-old male broilers were randomly allocated to 2 treatments and exposed to 25 and 35°C (RH, 50±5%) for 3 h. We observed that 3 h of heat exposure (35±1°C, 50±5% RH) increased the body temperature and respiratory rate of broiler chickens significantly, but plasma levels of corticosterone were not changed. Examination of [Ca2+]i and the proliferation of splenic lymphocytes isolated from heat-stressed broiler chickens, using fura-2-acetoxymethyl ester and Cell Counting Kit-8, respectively, showed that acute heat stress caused a significant increase in [Ca2+]i and enhanced concanavalin A-stimulated but not lipopolysaccharide-stimulated lymphocyte proliferation significantly. Flow cytometric analysis of the cell cycle and T-lymphocyte subsets (CD4+ and CD8+) indicated that heat stress promoted the transition of lymphocytes from gap phase 1 to synthesis phase and increased the ratio of CD4+ to CD8+ of T lymphocytes. In addition, acute heat stress enhanced the secretion of interleukin-2 by splenic lymphocytes significantly. These results suggest that the effect of acute heat stress to increase the [Ca2+]i in lymphocytes may be an early event that enhances Con A-stimulated T-cell proliferation and interleukin-2 secretion and promotes the transition of T cells from gap phase 1 to synthesis phase.