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 approximately 42 degrees C. This treatment led to a marked enhancement in lipopolysaccharide (LPS)-induced fever at 24 h after exposure to heat stress. The increase in fever was accompanied by a significant suppression in the circulating concentration of tumor necrosis factor. Heat-shock protein-70 measured in liver was elevated by the heat exposure (but not further elevated by the injection of LPS). An enhanced fever to LPS and other inflammatory stimuli found in heat-stressed human subjects could explain the apparent increase in susceptibility to disease.
Kluger
M J
MJ
Lovelace Respiratory Research Institute, Albuquerque 87108, USA.
Rudolph
K
K
Soszynski
D
D
Conn
C A
CA
Leon
L R
LR
Kozak
W
W
Wallen
E S
ES
Moseley
P L
PL
D000818:Animals; D001831:Body Temperature; D001833:Body Temperature Regulation; D001835:Body Weight; D003345:Corticosterone / Q000097:blood; D004926:Escherichia coli; D005334:Fever / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology*; D018840:HSP70 Heat-Shock Proteins / Q000096:biosynthesis; D006358:Hot Temperature; D006801:Humans; D007501:Iron / Q000097:blood; D008070:Lipopolysaccharides / Q000633:toxicity*; D008099:Liver / Q000378:metabolism; D008297:Male; D008954:Models, Biological; D051381:Rats; D017207:Rats, Sprague-Dawley; D013312:Stress, Physiological / Q000503:physiopathology*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D018840:HSP70 Heat-Shock Proteins; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D007501:Iron; D003345:Corticosterone