AI Article Synopsis
- The study found that the NLRP3 inflammasome helps protect mice from Enterovirus 71 (EV71) infections.
- Interleukin-18 (IL-18), which relies on the NLRP3 inflammasome, was identified as a key protective protein against EV71, as mice lacking IL-18 showed worse infections and higher viral loads.
- Administering recombinant IL-18 to mice that were deficient in IL-18 significantly reduced EV71 infection, suggesting IL-18 could be a potential treatment for hand, foot, and mouth disease linked to EV71.
Article Abstract
Previous study has demonstrated that the NLRP3 inflammasome is essential for protecting murine host against Enterovirus 71 (EV71) infection. However, the underlying mechanism remained unknown. Here we discovered that the pleiotropic cytokine interleukin-18 (IL-18), an NLRP3 inflammasome-dependent effector protein, exhibits a protective capability against EV71 challenge. Deficiency of IL-18 in mice exacerbated EV71 infection, which was reflected by increased viral replication, elevated production of interferons (IFN-β, IFN-γ), proinflammatory cytokines (TNF-α, IL-6) and chemokine CCL2,as well as decreased survival of experimental animals. Conversely, administration of recombinant IL-18 considerably restrained EV71 infection in IL-18 deficient mice. Thus, our results revealed a protective role for IL-18 against EV71 challenge, and indicated a novel therapeutic application for IL-18 in EV71 associated hand, foot, and mouth disease (HFMD).
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