[No authors listed]
Severe heat stroke (HS) consists of extreme hyperthermia with thermoregulatory failure, leading to high morbidity and mortality. Liver injury is a complication of HS that is associated with inflammatory responses and Kupffer cells (KCs), which are resident macrophages in the liver that serve as a major source of inflammatory cytokines; however, the association and the underlying mechanisms of KC functions in HSâinduced endotoxemia and inflammation require an improved understanding. The important chemokine macrophage inflammatory proteinâ1α (MIPâ1α) increases inflammatory responses and the secretion of inflammatory molecules from KCs, including tumor necrosis factorâα, interleukin (IL)â1β and ILâ6. In addition, the activation of câJun Nâterminal kinase (JNK) signaling is responsible for the development of liver inflammation. Therefore, HS animal and cell models were constructed in order to investigate the pathways involved in the HSâinduced dysfunction of KCs. The results of the present study suggest that JNK may be involved in the MIPâ1αâassociated pathogenesis of KCs in HS injury.
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