PPARγ mediated enhanced lipid biogenesis fuels <i>Mycobacterium tuberculosis</i> growth in a drug-tolerant hepatocyte environment.

ABSTRACT: Mycobacterium tuberculosis (Mtb) infection of the lungs, besides producing prolonged cough with mucus, also causes progressive fatigue and cachexia with debilitating loss of muscle mass. While anti-tuberculosis (TB) drug therapy is directed toward eliminating bacilli, the treatment regimen ignores the systemic pathogenic derailments that probably dictate TB-associated mortality and morbidity. Presently, it is not understood whether Mtb spreads to metabolic organs and brings about these impairments. Here, we show that Mtb creates a replication-conducive milieu of lipid droplets in hepatocytes by upregulating transcription factor PPARγ and scavenging lipids from the host cells. In hepatocytes, Mtb shields itself against the common anti-TB drugs by inducing drug-metabolizing enzymes. I

SUBMITTER: Sarkar B 

PROVIDER: S-EPMC12685304 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature