Heat stress triggers bone performance degeneration via impairing intestinal barrier function and altering gut...

Heat stress (HS) is a pervasive environmental hazard in intensive poultry production that severely impairs skeletal health and causes substantial economic losses. While emerging evidence links gut microbiota dysbiosis to bone metabolism, its causal role in mediating HS-induced bone loss remains poorly defined. Here, we established a chicken model of HS and employed fecal microbiota transplantation (FMT) to investigate the mechanistic link between gut microbiota and skeletal deterioration. Our results demonstrated that HS reduced growth performance, disrupted gut microbial community structure, and impaired bone microarchitecture and biomechanical strength. Critically, FMT from HS-exposed donors recapitulated the key features of HS-induced bone loss in recipient chickens, characterized by impaired trabecular bone microarchitecture, reduced biomechanical strength, and enhanced bone resorption-related gene expression. Mechanistically, the HS-microbiota induces functional dysbiosis, characterized by a relative increase in the abundance of the genus Turicibacter, while compromising intestinal barrier integrity, triggering an inflammatory response, and inhibiting intestinal mineral absorption. Collectively, these factors contribute to reduced bone performance. These findings establish the gut microbiota as a key mediator of HS-induced bone loss, providing a novel mechanistic framework for understanding host-microbiota-environment interactions in the context of environmental hazards, which has broader implications for animal health and environmental toxicology.