Abstract
We previously reported that levels of plasma corticosterone of rats in the alternatively changing ambient temperature (repeated temperature changes between 4 degrees and 27 degrees, each lasting for 1h) were higher than those in the constant low ambient temperature (4 degrees) at 1, 2, 4 and 10 days after the exposure. Frequently changing, but not constant, ambient temperatures may have induced a stronger stress. Furthermore LPS-induced fever in a group with high level of plasma corticosterone was enhanced. Plasma levels of TNF-α 3 h after LPS ( i.p. ) in animals exposed to constantly low and alternatively changing ambient temperatures for two days, tended to be higher than those exposed to constant 25 degrees temperature. Plasma levels of endotoxin in animals exposed to alternating ambient temperatures were higher than those exposed to constant 25 degrees and constant 4 degrees at 12 h and 2 days after the exposure. The possibility was considered that intrinsic endotoxin from enterobacterum leaked by stressful ambient temperature, and that leaked endotoxin primed macrophage resulting in enhanced fever. The aim of the present experiments was to ravel underlying mechanisms of the enhanced LPS-induced fever in animals exposed to stressful ambient temperatures. For this purpose, TNF-α production from rat peritoneal macrophages after the each ambient temperature exposure was observed, and the possibility of priming the cytokine productivity of macrophage by the intrinsic endotoxin is examined. [J Physiol Sci. 2008;58 Suppl:S107]
