Functional Analysis of SAA3 During Interaction Between Actinobacillus pleuropneumoniaeand Porcine Alveola Macrophages

Abstract

Abstract The spread of Porcine contagious pleuropneumonia (PCP), a severe disease that occurs in pigs caused by Actinobacillus pleuropneumoniae (APP), remains a threat to the porcine farms and has been known to cause severe economic losses. Serum amyloid A (SAA) is an acute-phase protein rapidly expressed in response to infection and inflammation in vertebrates. This study aimed to investigate the function of SAA3 in bacterial infections. Here, APP was used to infect porcine alveolar macrophages (3D4/21) and mice. The results showed that SAA3 expression was significantly upregulated in 3D4/21 cells and APP-infected mouse lung tissue. The expression of IL-1β, IL-6, and TNF-α were also upregulated in SAA3-overexpressing (SAA3-OE) cells. APP levels were substantially upregulated in the supernatant of SAA3-OE cells. Also, SAA3-OE promoted the adsorption and invasion of APP-infected target cells. These results suggested that porcine SAA3 promoted the proliferation of APP, providing insights into the role of porcine SAA3 in the course of bacterial infection.