Heat Stress Induces Inflammatory Response Through Inhibiting PPARα in Broiler Chickens

Heat stress poses a considerable challenge to the modern poultry industry by negatively impacting immune system maturation and eliciting inflammatory responses. Peroxisome proliferators-activated receptors α (PPARα), predominantly expressed in metabolically active tissues such as skeletal muscle, are essential for regulating the inflammatory process. Moreover, our recent research has found that heat stress down-regulates the transcription of PPARα in broiler chickens. To study if PPARα regulation is involved in heat-stress-induced skeletal muscle inflammatory response in broiler chickens, 180 male Arbor Acres (AA) broilers aged 22 days were randomly assigned to three experimental groups: a thermoneutral condition group at 21 °C, a heat stress group at 31 °C and a heat stress group at 31 °C supplemented with the PPARα activator fenofibrate. After 7 days of adaptive feeding, the broilers were subjected to a 14-day formal experimental phase. Results demonstrated that heat stress decreased the spleen and thymus index and increased serum and breast muscle inflammatory factor concentrations (p < 0.05). Moreover, heat-stress-induced abnormal breast muscle fiber morphology in broiler chickens. Furthermore, heat stress significantly up-regulated nuclear factor kappa-B (NF-κB) expression in boiler chickens (p < 0.05). However, activating PPARα through fenofibrate improved the growth performance (p < 0.05), enhanced immune organ indexes (p < 0.05), reduced inflammatory factor concentrations (p < 0.05), alleviated breast muscle fiber morphology damage and suppressed NF-κB expression (p < 0.05) in the breast muscle of broiler chickens. Based on our previous research, these results collectively underscore that heat stress induced inflammation and up-regulated NF-κB in the breast muscle of broiler chickens by inhibiting PPARα.