The gut–brain–mitochondria axis in heat-stressed poultry: Mechanisms and implications for health and productivity
TL;DR
This review synthesises current evidence on heat stress-induced disruption of the GBMA at multiple levels, including gut architecture and microbiota, neuroendocrine regulation, and mitochondrial function, and highlights how maladaptive feedback loops involving inflammation and oxidative stress exacerbate physiological dysfunction, ultimately reducing productivity, resilience, and welfare in poultry.
Abstract
Abstract Heat stress remains a major constraint to global poultry production, with profound implications for bird health, welfare, and productivity. Exposure to elevated ambient temperatures disrupts thermoregulation, metabolism, immune competence, and behaviour, ultimately compromising performance and survival. Growing evidence indicates that the gut–brain–mitochondria axis (GBMA) represents a critical integrative network through which birds perceive, respond to, and adapt to thermal stress. Heat stress-induced impairment of intestinal barrier integrity, dysbiosis of the gut microbiota, and altered secretion of gut-derived metabolites and neuroactive compounds converge on neuroendocrine pathways, particularly the hypothalamic–pituitary–adrenal and sympathetic axes, thereby modulating appetite regulation, stress reactivity, and thermoregulatory behaviour. Concurrently, excessive production of reactive oxygen species and calcium imbalance in mitochondria-rich tissues disrupt mitochondrial dynamics and bioenergetics, promoting oxidative damage and apoptosis. This review synthesises current evidence on heat stress-induced disruption of the GBMA at multiple levels, including gut architecture and microbiota, neuroendocrine regulation, and mitochondrial function. We further highlight how maladaptive feedback loops involving inflammation and oxidative stress exacerbate physiological dysfunction, ultimately reducing productivity, resilience, and welfare in poultry.