Human metapneumovirus activates NOD-like receptor protein 3 inflammasome via its small hydrophobic protein which plays a detrimental role during infection in mice.

摘要: NOD-like receptor protein 3 (NLRP3) inflammasome activation triggers caspase-1 activation-induced maturation of interleukin (IL)-1β and IL-18 therefore is important for the development host defense against various RNA viral diseases. However, implication this complex in human metapneumovirus (HMPV) disease has not been fully studied. Herein, we report that NLRP3 plays a detrimental role during HMPV infection because inhibition protected mice from mortality reduced weight loss inflammation without impacting replication. We also demonstrate exerts its deleterious effect via IL-1β production since observed mortality, IL-1β-deficient (IL-1β-/-) mice, as compared to wild-type animals infection. Moreover, on these evaluated parameters was different IL-1β-/- treated with an inhibitor. The abrogated bone marrow derived macrophages deficient NLRP3. Finally, show small hydrophobic protein-deleted recombinant (HMPV ΔSH) failed activate caspase-1, which responsible cleavage maturation. Furthermore, ΔSH-infected had less loss, showed no inflammation, HMPV-infected mice. Thus, seems be triggered by SH disease. In summary, once activated protein, promotes IL-1β, exacerbates HMPV-induced inflammation. Therefore, blockade using inhibitors might novel potential strategy therapy prevention