Project description:To compare gene expression changes induced by infection with Mycobacterium tuberculosis (Mtb) with changes induced by purified Mtb products, we infected THP-1 cells with Mtb strain H37Rv or treated with purified Mtb products, then performed RNAseq.
Project description:Comparison of gene expression profile of the whiB4 mutant strain of Mycobacterium tuberculosis with the wild type Mycobacterium tuberculosis H37RV Mtb WhiB4 mutant mRNA was compared with the mRNA of wtMtb H37RV under aerobic conditons Aerbic conditions OD600 nm of 0.4, MtbWhiB4KO vs wtMtb, biological replicates: 3 wt Mtb H37RV and 3 MtbWhiB4 KO
Project description:Comparison of gene expression profile of the whiB4 mutant strain of Mycobacterium tuberculosis with the wild type Mycobacterium tuberculosis H37RV Mtb WhiB4 mutant mRNA was compared with the mRNA of wtMtb H37RV under aerobic conditons
Project description:Mycobacterium tuberculosis(Mtb) is known to reside in cells of innate immune system- macrophages and dendritic cells. A variety of non -conventional cell typeslike adipocytes, mesenchyal stem cells and osteoclasts can also be infected with Mtb. However, cellular transcriptional adapations enabling survival of Mtb in these cells remain known. We used microarrays to understand global changes in transcriptional profiling during macrophage to osteoclast transition in presence of Mycobacterium tuberculosis.
Project description: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.
Project description:Mycobacterium tuberculosis (Mtb) displayed cording phenotypes during intracellular infection. RNA-Seq was used to identify transcriptional programmes expressed by hLEC that actviates pathways relating to cellular pro-survival and cyosolic surveillance of intracellular Mtb. Mtb cording was found to be a mechanism to evade xenophagy in the cytosol of endothelial cells.
Project description:The ability of Mycobacterium tuberculosis (Mtb) to adopt heterogeneous physiological states, underlies it’s success in evading the immune system and tolerating antibiotic killing. Drug tolerant phenotypes are a major reason why the tuberculosis (TB) mortality rate is so high, with over 1.8 million deaths annually. To develop new TB therapeutics that better treat the infection (faster and more completely), a systems-level approach is needed to reveal the complexity of network-based adaptations of Mtb. Here, we report the transcriptional response of Mtb to the drug pretomanid. We performed transcriptomic sequencing (RNA-seq) on Mtb bacilli at 4, 24, 72 h following exposure to the drug.
