Heat stroke activates a stress-induced cytokine response in skeletal muscle.
Level 5 - mechanism / opinion, no new human data
Preclinical animal experimental research
PubMed 23928112 · doi:10.1152/japplphysiol.00636.2013
What was done
Conscious mice were heated to a core temperature of 42.4°C to induce heat stroke. Diaphragm and hindlimb muscles were sampled throughout recovery to assess mRNA and protein expression of cytokines (IL-6, IL-10, TNF-α, IL-1β), toll-like receptors (TLR-2, TLR-4), heat shock proteins (HSP-72, HSP25), and transcription factor subunits (c-jun, c-fos).
What was found
No numerical values were provided in the abstract. Heat stroke led to a rapid rise in IL-6 and IL-10 mRNA and transient inhibition of TNF-α and IL-1β mRNA in both diaphragm and hindlimb muscles. IL-6 protein was transiently elevated in both muscle beds at ~32 minutes after reaching peak core temperature. TLR-4, HSP-72, c-jun, and c-fos mRNA were upregulated, whereas TLR-2 and HSP25 mRNA showed no change. At 24 hours, a secondary increase in IL-6, IL-10, IL-1β, and TNF-α protein occurred in hindlimb muscle but not in the diaphragm.
Why it matters
This study indicates that skeletal muscle actively participates in the systemic cytokine response during heat stroke via a distinct stress-induced pathway, rather than acting merely as an innocent bystander.
Limits
The abstract reports no sample size, control group specifications, or quantitative effect sizes and confidence intervals. Findings in conscious mice may not directly translate to human clinical heat stroke.
Cited by
- supports Severe heat shock in rodents induces massive muscle-derived IL-6 release into circulation that suppresses TNF and IL-1.