Myeloid Protease-Activated Receptor-2 Contributes to Influenza A Virus Pathology in Mice.

ABSTRACT:

Background

Innate immune responses to influenza A virus (IAV) infection are initiated in part by toll-like receptor 3 (TLR3). TLR3-dependent signaling induces an antiviral immune response and an NFκB-dependent inflammatory response. Protease-activated receptor 2 (PAR2) inhibits the antiviral response and enhances the inflammatory response. PAR2 deficiency protected mice during IAV infection. However, the PAR2 expressing cell-types contributing to IAV pathology in mice and the mechanism by which PAR2 contributes to IAV infection is unknown.

Methods

IAV infection was analyzed in global (Par2^-/- ), myeloid (Par2 ^fl/fl;LysM^Cre+) and lung epithelial cell (EpC) Par2 deficient (Par2^fl/fl ;SPC^Cre+) mi

SUBMITTER: Gunther RC 

PROVIDER: S-EPMC8671937 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature