Project description:Transcriptional profiling of mycobacterium tuberculosis clinical isolates in China comparing extensively drug-resistant tuberculosis with drug sensitive one.
Project description:Extensively drug resistant tuberculosis (XDR-TB) showed many different characteristics including the extreme drug resistance versus the drug sensitive clinical isolates (DS-TB), to know better about the reasons we used the tuberculosis host cells named as THP-1 (one kind of the macrophage cells) to be infected by the XDR-TB and DS-TB.DS strain A36 and the XDR strain B42 and was typical and selected by our lab. Then the total RNA of infected or uninfected THP-1 cells was extract and purified for the analysis by the chip (22K Human Genome chip representing the 21522 ORF of human with the oligonucleotide probe of 70 mer from CapitalBio Corp., Beijing, China). The results reflected the different expressed genes involved in apoptosis, secreted cytokines and signal pathway and so on. Those results might indicate the how the XDR-TB cause the pathogenesis.
Project description:Transcriptional profiling of mycobacterium tuberculosis clinical isolates in China comparing extensively drug-resistant tuberculosis with drug sensitive one. The same condition experiment. The samples were from the different drug-resistant strains. Only one replicate.
Project description:Tuberculosis (TB) remains a deadly disease. The genetic diversity of Mycobacterium tuberculosis was neglected in the past, but is increasingly recognized as a determinant of immune responses and clinical outcomes of TB. However, how this bacterial diversity orchestrates immune responses to direct differences in TB severity remains unknown. We studied 681 patients with pulmonary TB and found that phylogenetically related M. tuberculosis isolates from cases with mild disease induced robust cytokine responses in macrophages. In contrast, isolates associated with severe TB cases failed to do so. Using representative isolates, we show that M. tuberculosis inducing a low cytokine response in macrophages also diminished activation of cytosolic surveillance systems, including cGAS and the inflammasome, suggesting a novel mechanism of immune escape. Isolates exhibiting this evasion strategy carried mutations in various components of the ESX-I secretion system. We conclude that host interactions with different M. tuberculosis strains results in variable TB severity.
