Cytokines are intracellular peptides that serve as immune mediators. The levels of both pro- and anti-inflammatory cytokines have been demonstrated to rise in the event of heat stroke in both human and animal models. Different hyperthermic states, including both normal exercise-induced hyperthermia and classical and exertional heat stroke, result in unique characteristic profiles of plasma cytokines. The complexity of the interaction between pro- and anti-inflammatory cytokines is outlined in the vast number of experimental studies and clinical observations reported in the literature. However, there is no unanimous logic in studying the changes in cytokine levels, and therefore, it is difficult to compare the effects seen in the different reports. The strong inflammatory response to heat stroke increases after the cessation of heat stress and is intricately involved both in damage-generating processes and in repair mechanisms that are put into action during the recovery phase. In surviving individuals, this response diminishes in magnitude as time progresses and eventually subsides to allow return-to-normal homeostasis. A greater magnitude of the inflammatory response is often associated with poor prognosis and even fatalities, suggesting an imbalance of the immune system, which causes an unregulated inflammatory response. This review describes the common known processes relating to the predominant cytokines altered in the event of heat injury. The role of cytokines, specifically in the pathophysiology of heat stroke, is elaborated and depicted as part of a biaxial model pertaining to the physiological and cellular/biochemical aspects of heat stroke.

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