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- W4281567326 abstract "Sepsis is characterized by systemic inflammation, it's caused by primary infection of pathogenic microorganisms or secondary infection of damaged tissue. In this study, we focus on sepsis-induced intestine barrier functional disturbalice, presenting as increased permeability of intestinal epithelium. We observed that the phenotype of LPS-induced sepsis was exacerbated in Card9-/- mice, especially displaying more serious intestinal inflammation and gut barrier dysfunction. Next, we found the hyperactivation of NLRP3 inflammasome in the intestinal macrophages of Card9-/--sepsis mice. Moreover, Card9 over-expression decreased NLRP3 inflammasome activation in macrophages. Furthermore, we found that Card9 inhibited NLRP3 inflammasome activation by recruiting Ripk2. The competitive binding between Ripk2 with Caspase-1, instead of ASC with Caspase-1, inhibited the NLRP3 inflammasome activation. Over-expression of Ripk2 alleviated septic intestinal injury caused by Card9 deficiency. Taken together, we suggested Card9 acts as a negative regulation factor of NLRP3 inflammasome activation, which protects against intestinal damage during sepsis. Therefore, maintaining Card9-Ripk2 signaling homeostasis may provide a novel therapy of septic intestinal damage." @default.
- W4281567326 created "2022-05-27" @default.
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- W4281567326 date "2022-05-26" @default.
- W4281567326 modified "2023-10-17" @default.
- W4281567326 title "Card9 protects sepsis by regulating Ripk2-mediated activation of NLRP3 inflammasome in macrophages" @default.
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- W4281567326 doi "https://doi.org/10.1038/s41419-022-04938-y" @default.
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