Actinobacillus pleuropneumoniae infection activates IL-1β expression in porcine alveolar macrophage by promoting β-amyloid production

Abstract

Abstract Actinobacillus pleuropneumoniae (A. pleuropneumoniae) is a porcine respiratory tract pathogen and causes porcine pleuropneumonia. Porcine alveolar macrophage plays an important role during A. pleuropneumoniae infection. Amyloid precursor protein (APP) can be cleaved by β- and γ-secretase to produce β-amyloid (Aβ). APP and Aβ are related with inflammatory response. They activate micriglia and astrocyte to secrete IL-1β, IL-6 and other cytokines. In present study, we find that during interaction of A. pleuropneumoniae and porcine alveolar macrophage, two component system CpxAR upregulates wecA expression to increase lipopolysaccharide production, lipopolysaccharide promotes amyloid precursor protein (APP) production and cleavage to generate Aβ; the Aβ activates NF-κB leading to increased IL-1β expression. We present a hypothesis about A. pleuropneumoniae infection porcine alveolar macrophage regulates APP production and cleavage to control the quantity of Aβ; different quantities of Aβ induce PAMs produce different quantities of cytokines and leading to different pathological process of porcine pleuropneumonia.