Hyperthermia induces IL-1α but does not decrease release of IL-1α or TNF-α after endotoxin

D. Blake, P. Bessey, I. Karl, I. Nunnally, R. Hotchkiss

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


Heat treatments administered prior to the onset of sepsis or endotoxemia markedly increase survival. A potential mechanism for the beneficial effect of heat could be effects on IL-1α and TNF-α, important mediators of sepsis and endotoxemia. Administration of IL-1 or TNF prior to development of sepsis and endotoxemia increases survival; thus, prophylactic heat treatments may protect by releasing IL-1 or TNF. Paradoxically, an alternative mechanism of protection of prophylactic heat treatments could be to decrease the amount of IL-1 and TNF released during sepsis or endotoxemia. Cells pretreated with heat do not produce as much IL-1 or TNF in response to endotoxin as cells that have not been pretreated with heat. The purpose of this investigation was to determine if hyperthermia caused release of cytokines and/or blunted the rise in cytokines occurring after endotoxin. Mice were anesthetized with ketamine/xylazine and immersed in a water bath at 37.0 or 42.0°C for sham or heat treatments. At 6-7 h after recovery from anesthesia and immersion, sham and heat-treated mice were injected with Escherichia coli endotoxin. Both heat-treated and sham mice had elevated plasma IL-1α 2 h after anesthesia and immersion but IL-1α was ~3-fold greater in the heated mice, 732 ± 50 vs. 256 ± 76 pg/ml (p < 0.01). Blood samples obtained after endotoxin revealed no difference in levels of TNF-α (5477 ± 742 vs. 6514 ± 652 pg/ml) or IL-1α (546 ± 72 vs. 603 ± 121 pg/ml) in the sham vs. heated mice. We concluded that hyperthermia causes induction of IL-1α but not TNF- α and that increases in IL-1α may be an important mechanism for the beneficial effects of prophylactic heat treatments on survival in sepsis and endotoxemia.

Original languageEnglish
Pages (from-to)271-275
Number of pages5
JournalLymphokine and Cytokine Research
Issue number5
StatePublished - 1994


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