Neuroinflammation induced by secretion of acetylated HMGB1 from activated microglia in hippocampi of mice following chronic cold exposure.

Stress is a nonspecific response to adverse circumstances and chronic stress can destroy homeostasis, leading to various primary diseases. Although chronic cold stress is becoming increasingly important for individuals living or working in extreme environments, the risk of associated disorders of the central nervous system remains unstudied. Here, male C57BL/6 mice were exposed to a temperature of 4 °C, for three hours each day for one, two or three weeks. Glial cell activation, neuronal structure, and neuroinflammation were then evaluated by western blotting, immunofluorescence, Nissl staining and co-immunoprecipitation. Microglial activation, accompanied by activation of the NF-κB signaling pathway, release of pro-inflammatory cytokines and loss of Nissl bodies, was observed in mouse hippocampal tissue following cold exposure. We speculate that these phenomena are mediated by the HMGB1/TLR4/NF-κB pathway and closely associated with acetylation of HMGB1 in the hippocampus. These findings provide new insights into the mechanisms of the cold stress response, which should inform the development of new strategies to combat the effects of hypothermia.

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