Heat stress is a global issue for the poultry industries with substantial annual economic losses and threats to bird health and welfare. When chickens are exposed to high ambient temperatures, like other species they undergo multiple physiological alterations, including behavioral changes, such as cessation of feeding, initiation of a stress signaling cascade, and intestinal immune, and inflammatory responses. The brain and gut are connected and participate in bidirectional communication via the nervous and humoral systems, this network collectively known as the gut-brain axis. Moreover, heat stress not only induces hyperthermia and oxidative stress at the gut epithelium, leading to impaired permeability and then susceptibility to infection and inflammation, but also alters the composition and abundance of the microbiome. The gut microflora, primarily via bacterially derived metabolites and hormones and neurotransmitters, also communicate via similar pathways to regulate host metabolic homeostasis, health, and behavior. Thus, it stands to reason that reshaping the composition of the gut microbiota will impact intestinal health and modulate host brain circuits via multiple reinforcing and complementary mechanisms. In this review, we describe the structure and function of the microbiota-gut-brain axis, with an emphasis on physiological changes that occur in heat-stressed poultry.
Keywords: anorexia; heat stress; immune response; microbiota-gut-brain axis; poultry.
Copyright © 2021 Cao, Chowdhury, Cline and Gilbert.