Abstract
Abstract Activation of the inflammasome leads to caspase-1 activation and maturation of pro-inflammatory cytokines, IL-1β and IL-18. The inflammasome plays a pivotal role in host defense against microbial pathogens. However, its uncontrolled activation is associated with inflammatory disorders, suggesting that regulation of inflammasome activation is important to prevent detrimental effects. In this study, we found that endogenous and exogenous NO inhibits the NLRP3 inflammasome. iNOS was involved in the regulation of NLRP3 inflammasome activation by either IFN-β pretreatment or long-term LPS stimulation. Furthermore, the NO donor SNAP markedly inhibited NLRP3 inflammasome activation, while the AIM2 and NLRC4 inflammasomes were only partially inhibited by SNAP. An increase in mitochondrial reactive oxygen species induced by ATP was only modestly affected by SNAP treatment. S-nitrosylation of NLRP3 was detected in macrophages treated with SNAP, and this modification may account for the NO-mediated mechanism controlling inflammasome activation. Taken together, these results revealed a novel role of NO in regulating the NLRP3 inflammasome.
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