Impaired fatty acid import or catabolism in macrophages restricts intracellular growth of <i>Mycobacterium tuberculosis</i>.

ABSTRACT: Mycobacterium tuberculosis (Mtb) infection of macrophages reprograms cellular metabolism to promote lipid retention. While it is clearly known that intracellular Mtb utilize host derived lipids to maintain infection, the role of macrophage lipid processing on the bacteria's ability to access the intracellular lipid pool remains undefined. We utilized a CRISPR-Cas9 genetic approach to assess the impact of sequential steps in fatty acid metabolism on the growth of intracellular Mtb. Our analyzes demonstrate that macrophages which cannot either import, store or catabolize fatty acids restrict Mtb growth by both common and divergent anti-microbial mechanisms, including increased glycolysis, increased oxidative stress, production of pro-inflammatory cytokines, enhanc

SUBMITTER: Simwela NV 

PROVIDER: S-EPMC11291043 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature