Abstract

Heatstroke causes acute injury and damage across numerous organ systems, during this process, inflammation drives disease progression. In this study, we correlated temporal changes in inflammatory response with barrier breakdown within 24 hours following heatstroke onset to explore whether inflammation in circulation can influence inflammation in brain. We found both proinflammatory cytokines expression and pathological lesions in tissue were elevated at 1 h and 6 h after heatstroke onset. However, by 24 h after heatstroke onset, while systemic inflammation was sustained at high levels, neuroinflammation and cerebral cortex damage had returned to the level of control group. Change in microglial phenotype from classic activation after 1 h to alternative activation by 24 h post heatstroke onset may explain why neuroinflammation returned to baseline by 24 h post heatstroke onset. Taken together, our results indicate microglial phenotype transformation drives neuroinflammation independent of systemic inflammation during the acute stage of heatstroke.