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

D Blake¹, P Bessey, I Karl

¹Department of Surgery, Washington University School of Medicine, St. Louis, MO 63110.

Lymphokine and Cytokine Research

|October 1, 1994

Summary

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Pre-sepsis heat treatment boosts survival by altering inflammatory responses. Hyperthermia increases interleukin-1 alpha release but does not affect tumor necrosis factor-alpha levels during endotoxemia.

Area of Science:

Immunology
Physiology
Sepsis Research

Background:

Pre-sepsis heat treatments significantly improve survival rates.
Interleukin-1 alpha (IL-1 alpha) and Tumor Necrosis Factor-alpha (TNF-alpha) are key mediators in sepsis and endotoxemia.
Prophylactic heat may protect by releasing or reducing these cytokines.

Purpose of the Study:

To investigate if hyperthermia induces cytokine release.
To determine if hyperthermia blunts the cytokine response to endotoxin.

Main Methods:

Mice underwent sham or heat (42.0°C) treatments under anesthesia.
Escherichia coli endotoxin was administered 6-7 hours post-treatment.
Plasma cytokine levels (IL-1 alpha, TNF-alpha) were measured via ELISA.

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Main Results:

Both groups showed elevated IL-1 alpha post-anesthesia, with heated mice having ~3-fold higher levels (732 pg/ml vs. 256 pg/ml).
Post-endotoxin, no significant differences in TNF-alpha or IL-1 alpha levels were observed between sham and heated mice.

Conclusions:

Hyperthermia prior to endotoxin challenge causes an initial surge in IL-1 alpha.
Heat treatment does not appear to blunt the subsequent rise in IL-1 alpha or TNF-alpha during endotoxemia.