EphA2 phosphorylates NLRP3 and inhibits inflammasomes in airway epithelial cells.

ABSTRACT: Inflammasomes are intracellular complexes that form in the cytosol of inflammatory cells. NLRP3 is one of the sensor proteins in the complex that can recognize a wide variety of stimuli ranging from microbial components to environmental particulates. Here, we report that in mouse airway epithelial cells (AECs), inflammasome activation is inhibited by EphA2, a member of the transmembrane tyrosine kinase receptor family, via tyrosine phosphorylation of NLRP3 in a model of reovirus infection. We find that EphA2 depletion markedly enhances interleukin-1β (IL-1β) and interleukin-18 (IL-18) production in response to the virus. EphA2^-/- mice show stronger inflammatory infiltration and enhanced inflammasome activation upon viral infection, and aggravated asthma symptoms upon ovalbumin (

SUBMITTER: Zhang A 

PROVIDER: S-EPMC7332978 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature