Heat stress-induced gut dysbiosis and multi-organ injury: mechanisms and therapeutic modulation
TL;DR
It is suggested that gut microbiota dysbiosis may act as a mediator and amplifier of HS-induced pathology, and Targeting the gut-organ axis through probiotics, prebiotics, antioxidants, or functional amino acids offers promising but largely preclinical adjunctive strategies.
Abstract
Heat stress (HS) is an increasingly prevalent environmental and exertional challenge. In severe cases, HS may progress to heatstroke, a life-threatening clinical syndrome characterized by severe hyperthermia, systemic inflammation, and multi-organ dysfunction. This review synthesizes evidence from laboratory rodent models and suggests that gut microbiota dysbiosis may act as a mediator and amplifier of HS-induced pathology. Across diverse rodent models, HS remodels the gut microbiota by reducing microbial diversity. These compositional changes are accompanied by decreased short-chain fatty acids, altered bile acid profiles, and increased lipopolysaccharide burden, although the specific metabolites affected vary across models. Causal evidence from fecal microbiota transplantation and gnotobiotic experiments supports microbiota-dependent amplification of intestinal barrier failure, hepatic inflammation, and neuroinflammation. In contrast, evidence for the gut-reproductive, gut-kidney, gut-heart, gut-muscle, and gut-adipose axes remains predominantly associative or derived from interventional correlations without formal causality testing. Targeting the gut-organ axis through probiotics, prebiotics, antioxidants, or functional amino acids offers promising but largely preclinical adjunctive strategies, with rapid cooling and supportive care remaining the foundation of heatstroke management. Future research should prioritize temporally resolved human studies, multi-omics integration, and causal validation to define the translational potential of microbiome-directed interventions.