Transciptomic changes in Mycobacterium tuberculosis (Mtb) infected hepatocytes at early and late time points of infection
Mycobacterium tuberculosis (Mtb), although primarily a pulmonary pathogen, can disseminate to various other organs of the body causing extra pulmonary tuberculosis (EPTB). In the present study, we have shown that hepatocytes, the major parenchyma cells of the liver, get robustly infected by Mtb. Using a combination of in-vitro, ex-vivo and animal models; we demonstrate that Mtb utilizes hepatocytes as a replicative niche, modulates its various biological functions like lipid metabolism and shields itself against the common anti-TB drugs. Hepatocytes, being a key cell type having both immune and metabolic functions, controls and coordinates various aspects of the physiology in both health and disease. In case of a multifactorial chronic infection like TB, we are curious to know whether hepatocyte infection plays any major role in the systemic outcome of this age-old disease. Overall design: HepG2 cell lines were infected with Mtb-H37Rv-mCherry at a multiplicity of infection of 10 (MOI:10) . Two time points were selected:- early time point of 0 hour post infection ( i.e., 5 hours of incubating the cells with Mtb) and late time point of 48 hours post infection (i.e., 48 hours ). After infection, a single cell suspension was made and only the mCherry positive HepG2 cells (infected) were sorted.