PPARdelta: A key modulator in the pathogenesis of diabetes mellitus and Mycobacterium tuberculosis co-morbidity.

ABSTRACT: The interplay between lipid metabolism and immune response in macrophages plays a pivotal role in various infectious diseases, notably tuberculosis (TB). Herein, we illuminate the modulatory effect of heat-killed Mycobacterium tuberculosis (HKMT) on macrophage lipid metabolism and its implications on the inflammatory cascade. Our findings demonstrate that HKMT potently activates the lipid scavenger receptor, CD36, instigating lipid accumulation. While CD36 inhibition mitigated lipid increase, it unexpectedly exacerbated the inflammatory response. Intriguingly, this paradoxical effect was linked to an upregulation of PPARδ. Functional analyses employing PPARδ modulation revealed its central role in regulating both lipid dynamics and inflammation, suggesting it as a potential therapeu

SUBMITTER: AlSaeed H 

PROVIDER: S-EPMC11233913 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature