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Non-canonical inflammasome activation is crucial in the development of septic shock promoting pyroptosis and proinflammatory cytokine production via caspase-11 and gasdermin D (GSDMD). Here, we show that NAD\n                    <jats:sup>+<\/jats:sup>\n                    treatment protected mice toward bacterial and lipopolysaccharide (LPS)-induced endotoxic shock by blocking the non-canonical inflammasome specifically. NAD\n                    <jats:sup>+<\/jats:sup>\n                    administration impeded systemic IL-1\u03b2 and IL-18 production and GSDMD-mediated pyroptosis of macrophages via the IFN-\u03b2\/STAT-1 signaling machinery. More importantly, NAD\n                    <jats:sup>+<\/jats:sup>\n                    administration not only improved casp-11 KO (knockout) survival but rendered wild type (WT) mice completely resistant to septic shock via the IL-10 signaling pathway that was independent from the non-canonical inflammasome. Here, we delineated a two-sided effect of NAD\n                    <jats:sup>+<\/jats:sup>\n                    blocking septic shock through a specific inhibition of the non-canonical inflammasome and promoting immune homeostasis via IL-10, underscoring its unique therapeutic potential.\n                  <\/jats:p>","DOI":"10.7554\/elife.88686","type":"journal-article","created":{"date-parts":[[2023,8,16]],"date-time":"2023-08-16T08:39:54Z","timestamp":1692175194000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.88686","source":"Crossref","is-referenced-by-count":6,"title":["NAD+ prevents septic shock-induced death by non-canonical inflammasome blockade and IL-10 cytokine production in 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