Febrile-range temperatures achieved during sepsis and noninfectious SIRS correlate with detectable changes in stress gene expression in vivo, suggesting that fever can activate HSP gene expression and modify innate immune responses.
In high temperature (37 °C), heat shock protein (HSP) genes were the most co-regulated; other genes related with fatty acid metabolism, amino acid metabolism and transportation were also differentially expressed.
Our work demonstrated a promised method to enhance photothermal therapeutic effect, highlighting the importance of HSP inhibition and OH generation in promoting cell apoptosis under mild hyperthermia.