Background: The NLRP3 inflammasome is a significant component of the innate immune system that plays a vital role in the development of various parasitic diseases. However, its role in hepatic alveolar echinococcosis (HAE) remains unclear. Therefore, we aimed to investigate the NLRP3 inflammasome and its activation mechanism in HAE.Method: We assessed the expression of NLRP3, Caspase-1, interleukin (IL)-1β, and IL-18 in the inflammatory marginal zone and corresponding normal liver tissues of 60 patients with HAE. We used a rat model of HAE to investigate the role of the NLRP3 inflammasome in the inflammatory marginal zone of HAE. Transwell experiments were conducted to investigate the effect of Echinococcus multilocularis in stimulating Kupffer cells and hepatocytes. Further, immunohistochemical staining, western blotting, and ELISA assessed the expression of NLRP3 and Caspase-1, IL-1β, and IL-18, and flow cytometry was used to detect apoptosis and ROS.Results: The activation of NLRP3 inflammasome was intimately associated with the expression of ROS(P<0.05). Inhibition of ROS generation decreased the activation of NLRP3-Caspase-1-IL-1β pathway and mitigated damage to hepatocytes (P <0.01) as well as inflammation (P <0.001) in HAEConclusion: E. multilocularis can induce hepatocytes damage and inflammatory response by activating the ROS-NLRP3-Caspase-1-IL-1β pathway in Kupffer cells, indicating that ROS may be a potential target for the treatment of HAE.
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