EFFECT OF HEAT-STRESS ON LPS-INDUCED FEVER AND TUMOR-NECROSIS-FACTOR

Exposure to heat stress leads to both short-term and long-term effects on morbidity. Male rats were exposed to a high ambient temperature of 40 degrees C, which resulted in biotelemetered core body temperature rising to similar to 42 degrees C. This treatment led to a marked enha ncement in lipopolysaccharide (LPS)-induced fever at 24 h after exposu re to heat stress. The increase in fever was accompanied by a signific ant suppression in the circulating concentration of tumor necrosis fac tor Heat-shock protein-70 measured in liver was elevated by the heat e xposure (but not further elevated by the injection of LPS). An enhance d fever to LPS and other inflammatory stimuli found in heat-stressed h uman subjects could explain the apparent increase in susceptibility to disease.