Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1195367 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31645576_1.fastq.gz | Fastqsanger.gz | |||
| SRR31645576_2.fastq.gz | Fastqsanger.gz | |||
| SRR31645577_1.fastq.gz | Fastqsanger.gz | |||
| SRR31645577_2.fastq.gz | Fastqsanger.gz | |||
| SRR31645578_1.fastq.gz | Fastqsanger.gz |
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Project description:The cytokine IL-10 antagonizes pathways that control Mycobacterium tuberculosis (Mtb) infection. Nevertheless, the impact of IL-10 during Mtb infection has been difficult to decipher because loss of function studies in animal models have yielded only mild phenotypes. We have discovered that the transcription factor Bhlhe40 is required to repress Il10 expression during Mtb infection. Loss of Bhlhe40 in mice results in higher Il10 expression, higher bacterial burden, and early susceptibility similar to that observed in mice lacking IFN-g. Deletion of Il10 in Bhlhe40-/- mice reverses these phenotypes. Bhlhe40 deletion in T cells or CD11c+ cells is sufficient to cause susceptibility to Mtb. Bhlhe40 represents the first transcription factor found to be essential during Mtb infection to specifically regulate Il10 expression, revealing the importance of strict control of IL-10 production by innate and adaptive immune cells during infection. Our findings uncover a previously elusive but significant role for IL-10 in Mtb pathogenesis.
2018-05-09 | GSE113054 | GEO
Project description:How the complex interaction between Mycobacterium tuberculosis (Mtb) and the host is regulated during infection is still not well understood. Using a systems biology approach, we demonstrate here that miR-155 is one of several microRNAs that regulate host gene expression over the first 48 hours of Mtb infection in macrophages. miR-155 regulates the cell survival of Mtb-infected macrophages through SHIP1/AKT signaling. Using timecourse gene expression data, we constructed a miRNA regulatory network for the innate immune response to Mtb infection by WT macrophages. The network suggested a role for seven miRNAs in regulating the host response to Mtb, with miR-155 being one of them. We then validated a role for miR-155 by comparing the response between WT and miR-155-/- macrophages.
2016-09-14 | GSE79732 | GEO
Project description:How the complex interaction between Mycobacterium tuberculosis (Mtb) and the host is regulated during infection is still not well understood. Using a systems biology approach, we demonstrate here that miR-155 is one of several microRNAs that regulate host gene expression over the first 48 hours of Mtb infection in macrophages. miR-155 regulates the cell survival of Mtb-infected macrophages through SHIP1/AKT signaling. Using timecourse gene expression data, we constructed a miRNA regulatory network for the innate immune response to Mtb infection by WT macrophages. The network suggested a role for seven miRNAs in regulating the host response to Mtb, with miR-155 being one of them. We then validated a role for miR-155 by comparing the response between WT and miR-155-/- macrophages.
2016-09-14 | GSE79731 | GEO
Project description:Currently there is limited knowledge of changes in genome-wide chromatin accessibility during Mycobacterium tuberculosis (Mtb) infection and whether host phosphatases such as PPM1A play a role in this process. Using combinatorial chromatin accessibility (ATAC-seq) and transcriptomics (RNA-seq) profiling of wild-type (WT), PPM1A knockout (△PPM1A) and PPM1A overexpressing (PPM1A+) macrophages, we demonstrate that Mtb infection induces global chromatin remodeling consistent with changes in gene expression signatures. The strongest concordant chromatin accessibility and gene expression signature triggered by Mtb infection was enriched for genes involved in the type I interferon (IFN) signaling pathways. Modulation of PPM1A expression results in altered chromatin accessibility signatures during Mtb infection that are reflected in the total number, chromosome location and directionality of change.
2023-02-08 | GSE211976 | GEO
Project description:Mycobacterium tuberculosis (Mtb) secretes several virulence determinants that alter phagosome biogenesis, enabling its survival within the cell. Nevertheless, the mechanism underlying this process remains considerably obscure. Here, we have identified a novel regulatory mechanism whereby SIRT7 mediates Rac1 activation in cytoskeletal remodelling during Mtb infection. We found that SIRT7 are significantly decreased during Mtb infection in both mRNA and protein levels. SIRT7 deficiency impairs macrophage phagocytosis and bacteriacidal activity by disrupts actin cytoskeleton dynamics. In the murine TB model, the deficiency of Sirt7 had an adverse effect on the host's response to Mtb since it led to an increase in bacterial burden and inflammation in the lung. Conversely, the overexpression of Sirt7 impeded bacterial growth. Mechanistically, we have shown that SIRT7 limits Mtb infection by directly interacting with and activating RAC1. Therefore, we conclude that SIRT7 is responsible for driving cytoskeletal remodeling through RAC1, thus providing crucial insight into host response during Mtb infection and offering a potential target for tuberculosis treatment.
2023-12-20 | GSE245205 | GEO
Project description:Alveolar macrophages (AMs) are major targets of Mycobacterium tuberculosis (Mtb) infection, critical during the progression of active tuberculosis (TB). The complex immunopathology of TB generates diverse microenvironments in the lung, which shape immune responses by AMs. In the current study, we perform whole genome microarray transcriptional profiling on RNA isolated from AMs from TB patients (AMsTB) compared to AMs from control subjects (AMsCT) using bronchoalveolar lavage (BAL). Our hypothesis was that systemic effects on the local lung microenvironment during TB affect the transcriptional response of AMsTB. We found a unique gene expression profile of 51 genes, including up-regulated CHIT1, CHI3L1, CCL5, CCL22, CCL8, CXCL9, MMP9, MMP7 and MMP12, associated with a robust pro-inflammatory response, cell recruitment and tissue damage, and genes of the cyclin family (CCND1, CCND2, and CCNA1) associated with cell proliferation. These expression profiles may account for the inflammatory condition in the lungs of TB patients. CXCL5, IL1B, CAMP, and TGFB1 were down-regulated, suggesting an altered control of Mtb infection. Also, MARCO and COLEC12, affecting phagocytosis, and CES1, associated with an increase in free cholesterol, were down-regulated. The observed changes in mRNA expression profiles may partially account for the inability of AMsTB to effectively control Mtb infection, suggesting that a balanced control of pro- and anti-inflammatory immune responses is crucial for infection control.
2017-07-13 | GSE98750 | GEO
Project description:Monocytes play a critical role during infection with Mycobacterium tuberculosis (Mtb). They are recruited to the lung where they participate in the contention of infection. Alternatively, inflammatory monocytes may help in prolonging inflammation or serve as niches for Mtb infection. Also, monocyte response to infection may vary depending on the particularities of the clinical isolate of Mtb from which they are infected. In this pilot study, using microarrays we have examined the global mRNA profiles of circulating human monocytes from healthy individuals and patients with active tuberculosis (TB).
2020-04-21 | GSE139871 | GEO
Project description:Mycobacterium tuberculosis (Mtb)-induced shifts in macrophage metabolism are an accepted central infection paradigm. Mtb-infected murine lung tissue exhibits gene expression changes consistent with classic Warburg metabolism and Mtb-infected murine macrophages undergo TCA cycle remodeling. Human macrophages also respond energetically to Mtb infection, however, interestingly the phenotypic nature of this response appears to vary depending on the viability of infection. Despite the overwhelming consensus that metabolic changes are critical to the host response to infection, we have little understanding of the metabolic transcriptional landscape of virulent Mtb-infected human alveolar macrophages (AM), the sentinel pulmonary immune cell during Mtb infection. Further still, whether the human AM undergoes glycolytic reprogramming and TCA cycle remodeling during virulent Mtb infection remains undefined; as is suggested to occur in circulating Mtb-infected human macrophages. Here, we aimed to characterise the metabolic transcriptional profile of virulent Mtb-infected human AM. We hypothesised that infection would induce the transcriptome of Warburg metabolism (characterised by aerobic glycolysis), TCA cycle remodeling, and reduce expression of genes involved in mitochondrial oxidative phosphorylation (OXPHOS).
2025-05-15 | GSE266414 | GEO
Project description:Intervention type:DRUG. Intervention1:Huaier, Dose form:GRANULES, Route of administration:ORAL, intended dose regimen:20 to 60/day by either bulk or split for 3 months to extended term if necessary. Control intervention1:None.
Primary outcome(s): For mRNA libraries, focus on mRNA studies. Data analysis includes sequencing data processing and basic sequencing data quality control, prediction of new transcripts, differential expression analysis of genes. Gene Ontology (GO) and the KEGG pathway database are used for annotation and enrichment analysis of up-regulated genes and down-regulated genes.
For small RNA libraries, data analysis includes sequencing data process and sequencing data process QC, small RNA distribution across the genome, rRNA, tRNA, alignment with snRNA and snoRNA, construction of known miRNA expression pattern, prediction New miRNA and Study of their secondary structure Based on the expression pattern of miRNA, we perform not only GO / KEGG annotation and enrichment, but also different expression analysis.. Timepoint:RNA sequencing of 240 blood samples of 80 cases and its analysis, scheduled from June 30, 2022..
| 2612481 | ecrin-mdr-crc
Project description:Tuberculosis (TB) is one of the deadliest infectious disorders in the world. To effectively TB manage, an essential step is to gain insight into the lineage of Mycobacterium tuberculosis (MTB) strains and the distribution of drug resistance. Although the Campania region is declared a cluster area for the infection, to contribute to the effort to understand TB evolution and transmission, still poorly known, we have generated a dataset of 159 genomes of MTB strains, from Campania region collected during 2018-2021, obtained from the analysis of whole genome sequence data. The results show that the most frequent MTB lineage is the 4 according for 129 strains (81.11%). Regarding drug resistance, 139 strains (87.4%) were classified as multi susceptible, while the remaining 20 (12.58%) showed drug resistance. Among the drug-resistance strains, 8 were isoniazid-resistant MTB (HR-MTB), 7 were resistant only to one antibiotic (3 were resistant only to ethambutol and 3 isolate to streptomycin while one isolate showed resistance to fluoroquinolones), 4 multidrug-resistant MTB, while only one was classified as pre-extensively drug-resistant MTB (pre-XDR). This dataset expands the existing available knowledge on drug resistance and evolution of MTB, contributing to further TB-related genomics studies to improve the management of TB infection.
2023-11-17 | E-MTAB-13058 | biostudies-arrayexpress