Understanding heat stress as mediator of reduced bone health in broilers through its actions on bone cell proliferation and the “gut-bone” axis

Bone disorders such as tibial dyschondroplasia and lameness are highly prevalent in all poultry and broilers are no exception. Heat stress is well documented to have a negative influence on various livestock and its incidence is expected to increase. One of the noticeable developmental problems associated with heat stress is a pronounced induction in leg abnormalities in broilers and other poultry. Yet, the regulation of bone health by heat stress at the molecular level has not been clearly elucidated, preventing rational design of mitigation strategies. One of potential mechanisms is that heat stress directly acts on respective bone cells, i.e. osteoblasts and osteoclasts, by affecting Wnt/β-catenin and bone morphogenetic protein signaling pathways and affects the osteoblast-induced osteoclast development. Next, heat stress likely also regulates bone quality indirectly by alterations in the gut microbiota and/or intestinal barrier and host innate immunity, thus via the “gut-bone” axis. Dysbiosis and increased intestinal permeability has been thought to be a key contributor to the pathogenesis of bone disorders, but it is unclear whether heat stress can cause reduced bone health in a similar manner. This research aims to elucidate the role of heat stress as mediator of reduced bone health in broiler chickens. Findings will be confirmed in an intervention model with oral Lactobacillus reuteri and MDY, a high-molecular-weight polymer used as mucus supplement.