Pasteurella multocida.(PM) infection is a major cause of avian cholera, but the pathogenesis of the disease is unknown. The purpose of this study was to further understand the host response to infection by using a duck model of PM, 20 female ducks were divided into two groups (n = 10). One group was infected with PM, while the other served as an uninfected control group. The ducks were observed after infection and samples were collected for testing. In this study, we report the mechanism of PM-induced inflammation to further mediate apoptosis and autophagic signaling pathways in liver cells. Our results demonstrated that PM infection initially induces hemorrhagic and necrotic lesions in the liver tissue of duck, promoting inflammasome assembly and release, triggering inflammation. The TLR4/NF-κB axis activated and interacted with multiple inflammation-related proteins, including TNF-α and IL-1β, which affected apoptosis and autophagy. Tumor necrosis factor induced hepatocyte apoptosis was implicated in a wide range of liver diseases; the release of TNF-α and activation with NF-κB further incite apoptotic pathways,such as Bax/BCL2/caspase to promote apoptotic genes APAF1, Bax, Caspase3, BCL-2, p53, and Cytc expression. Finally, PM-induced autophagy suppressed liver injury by promoting the Beclin-1, LC3B, p62, and mTOR. Thus, liver injury caused by PM via promoting autophagy was induced. In conclusion, we analyzed the liver injury of ducks infected with PM, and confirmed that inflammation appeared in the liver; this was followed by the intricate interplay between inflammation, apoptosis, and autophagy signaling pathways. The observed results provided a reference basis for studying pathogenic mechanisms of PM-host interactions.
Keywords: Apoptosis; Autophagy; Inflammation; Liver injure; Pasteurella.
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