Tax1bp1 enhances bacterial virulence and promotes inflammatory responses during <i>Mycobacterium tuberculosis</i> infection of alveolar macrophages.

ABSTRACT: Crosstalk between autophagy, host cell death, and inflammatory host responses to bacterial pathogens enables effective innate immune responses that limit bacterial growth while minimizing coincidental host damage. Mycobacterium tuberculosis (Mtb) thwarts innate immune defense mechanisms in alveolar macrophages (AMs) during the initial stages of infection and in recruited bone marrow-derived cells during later stages of infection. However, how protective inflammatory responses are achieved during Mtb infection and the variation of the response in different macrophage subtypes remain obscure. Here, we show that the autophagy receptor Tax1bp1 plays a critical role in enhancing inflammatory cytokine production and increasing the susceptibility of mice to Mtb infecti

SUBMITTER: Chin J 

PROVIDER: S-EPMC11702572 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature