Project description:The capsular serotype has long been associated with the virulence of Streptococcus pneumoniae. Here we present an in-depth study of phenotypic and genetic differences between serotype 3 and serogroup 11 S. pneumoniae clinical isolates from both the general and indigenous populations of Australia. Both serotypes/groups included clonally unrelated strains with differences in well-known polymorphic virulence genes, such as nanA and pspA, as demonstrated by multilocus sequence typing and Western blot analysis. Nonetheless, the serotype 3 strains were consistently and significantly more virulent in mice than the serogroup 11 strains. Despite extensive genomic analysis, noncapsular genes common to one serotype/group but not the other were not identified. Nevertheless, following the conversion of a serotype 11A isolate to serotype 3 and subsequent analysis in an intranasal infection model, it was evident that both capsular and noncapsular factors determine the virulence phenotype in mice. However, it appears that these noncapsular factors vary from strain to strain. Data is also available from http://bugs.sgul.ac.uk/E-BUGS-126
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:To explore the mechanism of drug resistance, most works focused on resistance associated genetic mutations, whereas concerns for resistance related gene expression are relatively low. Here a global expression analysis was performed between a reference strain H37Rv and two clinical extensively drug-resistant (XDR) strains with three anti-TB drug exposures {isoniazid (INH), capreomycin (CAP), rifampicin (RIF)}
Project description:This study investigates the global transcriptional response of Streptococcus pneumoniae D39V (serotype 2 strain) to human blood components and CSF acquired from discarded and anonymized patient samples.
Project description:Mouse lung RNAseq after infection with Influenza A virus (H1N1, PR/8/34, mouse-adapted) and Streptococcus pneumoniae (serotype 19F, strain BHN 100) Results: Differentially expressed genes were observed after single and co-infection Project: COST_mouse_2021_lung
Project description:Mouse blood transcriptome after infection with Influenza A virus (H1N1, PR/8/34, mouse-adapted) and Streptococcus pneumoniae (serotype 19F, strain BHN 100) Results: Differentially expressed genes were observed after single and co-infection Project: COST_mouse_2021
Project description:<p><em>Streptococcus pneumoniae</em> is the primary cause of community-acquired bacterial pneumonia with rates of penicillin and multi-drug resistance exceeding 80% and 40%, respectively. The innate immune response generates a variety of antimicrobial agents to control infection including zinc stress. Here, we characterized the impact of zinc intoxication on <em>S. pneumoniae</em>, revealing disruptions in central carbon metabolism, lipid biogenesis and peptidoglycan biosynthesis. Characterization of the pivotal peptidoglycan biosynthetic enzyme GlmU revealed an exquisite sensitivity to zinc inhibition. Disruption of the sole zinc efflux pathway, czcD, rendered <em>S. pneumonia</em>e highly susceptible to β-lactam antibiotics. To dysregulate zinc homeostasis in the wild-type strain, we investigated the safe-for-human use ionophore PBT2. PBT2 rendered wild-type <em>S. pneumoniae</em> strains sensitive to a range of antibiotics. Using an invasive ampicillin-resistant strain, we demonstrate in a murine pneumonia infection model the efficacy of PBT2+ampicillin treatment. These findings present a therapeutic modality to break resistance of drug-resistant <em>S. pneumoniae</em>.</p>
2022-02-23 | MTBLS318 | MetaboLights
Project description:Extensively Drug-Resistant (XDR) Mycobacterium tuberculosis in Zhejiang, China
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. In this study, the well grown THP-1 cells were separated and cultured in three ampoules. Cells in one ampoules were infected with XDR-TB strain of B42. Cells in another ampoules were infected with DS-TB strain of A36, with the cells in the third one were not infected and just treated with PBS as the control. Then the dual channel method was used for detecting the hybridization of B42 vs the control or A36 vs control. This work was repeated for three times.