Cytokines and their role in hyperthermia and heat stroke

Abstract

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.

Splenic Gene Expression Signatures in Slow-Growing Chickens Stimulated in Ovo with Galactooligosaccharides and Challenged with Heat

“…During HS, the levels of both pro-inflammatory and anti-inflammatory cytokines increase. This is due to endotoxemia, which is a storm of microbial endotoxin (i.e., LPS-lipopolysaccharides) infiltrating the milieu of the body [56]. In the current study, slow-growing chickens that were subjected to chronic HS demonstrated a significantly higher expression of IL-10 and IL-12p40.…”

Characterization of kidney damage using several renal biomarkers in dogs with naturally occurring heatstroke

“…Heatstroke manifests as hyperthermia, tachypnea, panting, collapse, 61 shock, altered consciousness, seizures, vomiting, diarrhea, petechiae and ecchymosis (Bruchim 62 et al, 2006) parenchymal injury (Langston, 2010). The pathogenesis of heatstroke-associated AKI is most 70 likely multifactorial, and includes decreased perfusion due to dehydration and hypovolemia, 71 direct thermal injury, rhabdomyolysis-associated myoglobinuria and SIRS (Heled et al, 2013). 72…”

Multiple organ dysfunction due to heatstroke after sauna: case report and review of the literature

“…8 The mechanism underlying multiple organ dysfunction syndrome of heatstroke is not fully understood, but direct thermal injury to the endothelium, activation of the inflammatory and coagulatory pathways, tissue ischaemia and/or endotoxemia and cytokines have been suggested. 9,10 The key measures to maximise the survival chances of heatstroke patients are as follows: rapidly decreasing the elevated core body temperature and organ support of central nervous system, cardiovascular, pulmonary, renal system and the management of late or post-cooling complications. 11–13 After admission, our patient presented with acute renal injury, acute hepatic failure, skeletal muscle damage and disseminated intravascular coagulation soon.…”