Project description:Efforts to eradicate TB are largely threatened by drug-resistant tuberculosis, particularly, multidrug-resistant tuberculosis (MDR-TB). It is imperative to find one or more specific biomarkers for diagnosing MDR-TB earlier and declining the incidence. Growing evidences have showed lncRNAs are widely expressed and take part in the genesis and development of many diseases, including tuberculosis. Therefore, to screen the differential lncRNAs among MDR-TB, drug-sensitive tuberculosis(DS-TB) and healthy controls(HCs) is a good strategy to acquire potential biomarkers for MDR-TB diagnosis and partly describe the mechanism of MDR-TB. Here, the present study aimed to investigate the differential expression profile of lncRNAs in serum among patients with MDR-TB ,DS-TB and HCs using lncRNA microarray
Project description:A mass spectrometry strategy of parallel reaction monitoring was used to detect and validate differential proteins in serum. Here are the data including 3 groups of MDR-TB, DS-TB and HC.
Project description:The emergence of multidrug resistant (MDR) Mycobacterium tuberculosis (Mtb) strains, resistant to the frontline anti-tubercular drugs rifampicin and isoniazid, forces treatment with less effective and toxic second-line drugs and stands to derail TB control efforts. However, the immune response to MDR Mtb infection remains poorly understood. Here, we determined the RNA transcriptional profile of in vitro generated macrophages to infection with either drug susceptible Mtb HN878 or MDR Mtb W_7642 infection.
Project description:Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), latently infects one quarter of the world’s population. The rise of multidrug resistant (MDR) Mtb infections worldwide presents a significant obstacle to curb TB globally. While human studies report dysregulated immune responses in MDR TB patients, there is a lack of clear understanding of the host-pathogen interactions following MDR Mtb infection. We recently showed that Mtb carrying a rifampicin drug resistance (RDR)-conferring single nucleotide polymorphism in the RNA polymerase-B gene (Mtb rpoB-H445Y) can modulate host macrophage metabolic reprogramming by production of Type I IFNs. Here, using a mouse model, we have characterized the host immune response in vivo following RDR Mtb infection. We show that despite establishment of Mtb infection in the lung and dissemination to the peripheral organs, lung myeloid and lymphoid immune responses to RDR Mtb is suppressed through a Type I IFN-dependent mechanism. These results coincide with a muted responses in the bone marrow hematopoietic stem and progenitor cells (HSPCs) and progenitors following RDR Mtb infection. These results suggest that host directed therapeutics and vaccines for drug resistant TB may need to be target specific host immune pathways for protection.
Project description:We performed shallow whole genome sequencing (WGS) on circulating free (cf)DNA extracted from plasma or cerebrospinal fluid (CSF), and shallow WGS on the tissue DNA extracted from the biopsy in order to evaluate the correlation between the two biomaterials. After library construction and sequencing (Hiseq3000 or Ion Proton), copy number variations were called with WisecondorX.
Project description:A mass spectrometry strategy of data-independent acquisition was used to detect differential proteins in serum. Here are the data including 3 groups of MDR-TB, DS-TB and HC.
Project description:Whole genome sequencing (WGS) of tongue cancer samples and cell line was performed to identify the fusion gene translocation breakpoint. WGS raw data was aligned to human reference genome (GRCh38.p12) using BWA-MEM (v0.7.17). The BAM files generated were further analysed using SvABA (v1.1.3) tool to identify translocation breakpoints. The translocation breakpoints were annotated using custom scripts, using the reference GENCODE GTF (v30). The fusion breakpoints identified in the SvABA analysis were additionally confirmed using MANTA tool (v1.6.0).
Project description:Tuberculosis (TB) is still a major life-threatening infectious disease, within which especially the rise of multidrug resistant TB (MDR-TB) is currently worrying. This study focuses on mechanisms of development of rifampicin resistance, since rifampicin seems to play an important role in the development of MDR-TB. To provide further insight in rifampicin resistance, we performed a genome-wide transcriptional profile analysis for Mycobacterium tuberculosis (M. tuberculosis) using microarray technology and qRT-PCR analysis. We exposed a rifampicin-susceptible H37Rv wild type (H37Rv-WT) and a rifampicin-resistant progeny H37Rv strain with a H526Y mutation in the rpoB gene (H37Rv-H526Y) to several concentrations of rifampicin, to define the effect of rifampicin on the transcription profile. Our study showed that there are resistance-dependant differences in response between both M. tuberculosis strains. Gene clusters associated with efflux, transport and virulence were altered in the rifampicin-resistant H37Rv mutant compared to the rifampicin-susceptible H37Rv-WT strain after exposure to rifampicin. We conclude that the small gene cluster Rv0559c-Rv0560c in the H37Rv-H526Y strain was remarkably up-regulated in the microarray analysis and qRT-PCR results and appeared to be dependent on rifampicin concentration and time of exposure. Therefore this study suggests that Rv0559c and Rv0560c play a pivotal role in rifampicin resistance of M. tuberculosis. Further investigation of Rv0559c and Rv0560c is needed to reveal function and mechanism of both genes that were triggered upon rifampicin exposure. [Data is also available from http://bugs.sgul.ac.uk/E-BUGS-139]