The β2-adrenergic receptor modulates activity of porcine alveolar macrophages in response to Actinobacillus pleuropneumoniae infection

Actinobacillus pleuropneumoniae (APP) is a non-spore-forming, Gram-negative facultative, anaerobic bacterium frequently associated with piglet respiratory disease syndrome, which occurs at a notably higher incidence in the winter months and contributes to considerable economic losses to the global pig industry. Following APP infection, porcine lung tissues exhibit a robust inflammatory response characterized by the accumulation of porcine alveolar macrophages (PAMs), suggesting that the magnitude of the immune response elicited by PAMs is a critical determinant of the resolution of APP infection. Furthermore, the β2-adrenergic receptor (ADRB2) is predominantly expressed on the surface of PAMs, although the potential influence of ADRB2 on the immunological reactivity of PAMs post-APP infection remains unclear. Additionally, the regulatory effects of ADRB2 are closely associated with intracellular signaling of the cAMP-PKA pathway, which plays a pivotal role in shaping the immune response of PAMs.

The aim of this study was to elucidate the critical regulatory mechanisms underlying the influence of ADRB2 on the antibacterial immunity capacities of PAMs in order to provide a theoretical foundation for the development of ADRB2-based immunomodulatory strategies and offer new insights into the intricate regulatory network governing host antibacterial immunity in response to APP infection.