Inflammasome-mediated antagonism of type I interferon enhances Rickettsia pathogenesis.

ABSTRACT: The innate immune system fights infection with inflammasomes and interferons. Facultative bacterial pathogens that inhabit the host cytosol avoid inflammasomes^1-6 and are often insensitive to type I interferons (IFN-I), but are restricted by IFN-γ^7-11. However, it remains unclear how obligate cytosolic bacterial pathogens, including Rickettsia species, interact with innate immunity. Here, we report that the human pathogen Rickettsia parkeri is sensitive to IFN-I and benefits from inflammasome-mediated host cell death that antagonizes IFN-I. R. parkeri-induced cell death requires the cytosolic lipopolysaccharide (LPS) receptor caspase-11 and antagonizes IFN-I production mediated by the DNA sensor cGAS. The restrictive effects of IFN-I require the interferon regulatory

SUBMITTER: Burke TP 

PROVIDER: S-EPMC7239376 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature