Related Experiment Video
Updated: Dec 22, 2025
08:22
A Preclinical Model of Exertional Heat Stroke in Mice
Published on: July 1, 2021
4.2K
Prior viral illness increases heat stroke severity in mice
Shauna M Dineen1, Jermaine A Ward1, Lisa R Leon1
1US Army Research Institute of Environmental Medicine, Thermal Mountain Medicine Division, Natick, MA, USA.
Experimental Physiology
|May 4, 2020
Summary
Prior illness, particularly viral infections, increases heat stroke severity in mice by triggering ongoing inflammation and coagulation, not just higher body temperature. This suggests potential interventions targeting these pathways for better recovery.
Area of Science:
- Physiology
- Immunology
- Pathology
Background:
- Heat stroke (HS) is a severe condition potentially worsened by prior illness.
- Existing hypotheses suggest prior illness exacerbates HS by increasing hyperthermia or impairing cellular protection.
- This study investigates the mechanisms by which prior illness impacts HS severity.
Purpose of the Study:
- To determine if prior illness increases susceptibility and severity of heat stroke (HS).
- To elucidate the mechanisms underlying the exacerbation of HS by prior illness, focusing on hyperthermia, coagulation, and inflammation.
- To identify potential biomarkers and therapeutic targets for HS.
Main Methods:
- Male C57BL/6J mice were injected with viral (PIC) or bacterial (LPS) mimics, or saline.
- Mice underwent HS after 48 or 72 hours of recovery.
- Measurements included core body temperature, survival, platelet counts, cytokines, chemokines, and organ injury.
Main Results:
- Viral mimic (PIC) injection led to more severe HS outcomes, including reduced survival and increased duodenal injury, compared to controls.
- The exacerbation of HS by PIC was linked to persistent coagulation and inflammatory responses, not increased hyperthermia.
- Platelet counts and specific cytokines (RANTES, IP-10, IL-6, TNF-α) were altered during HS recovery in PIC-treated mice.
Conclusions:
- Prior illness, specifically viral mimic exposure, significantly increases HS severity in mice.
- The exacerbation is mediated by persistent systemic inflammation and coagulation, independent of hyperthermia.
- Platelets, cytokines, and chemokines may serve as indicators of HS susceptibility, with coagulation and inflammation as potential therapeutic targets.
