Mycobacterium avium complex (MAC)
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB12771 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR336772_1.fastq.gz | Fastqsanger.gz | |||
| DRR336772_2.fastq.gz | Fastqsanger.gz | |||
| DRR336773_1.fastq.gz | Fastqsanger.gz | |||
| DRR336773_2.fastq.gz | Fastqsanger.gz | |||
| DRR336774_1.fastq.gz | Fastqsanger.gz |
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Project description:We infected 18-month-old mice (old mice) and 9-week-old mice (young mice) with 1 × 10⁷ CFU of Mycobacterium avium via the respiratory tract for comparison analysis. Two months post-infection, both bacterial loads and mortality rates were significantly higher in old mice compared to young mice. RNA-seq analysis of lung tissues were performed.
2026-03-18 | GSE287501 | GEO
Project description:Mycobacterium avium complex (MAC) is a non-tuberculosis mycobacteria widely distributed throughout environment. Even though the MAC infection is currently increasing in old women and patients with affected immune system, comprehensive analysis of MAC-infected host cell transcriptome, in particular that of long non-coding RNAs (lncRNAs), has scarcely been reported. Using in vitro cultured primary mouse bone marrow-derived macrophages (BMDMs) and CAGE technology, we analyzed the transcriptional and kinetic landscape of macrophage genes, with focusing on lncRNAs, during MAC infection. MAC-infected macrophages induced immune/inflammatory response genes and other genes as similar as M1 activation, consistent with previous reports, although Nos2 and Arg1 revealed distinct expression profiles from M1 activation. We identified 31 up-regulated and 30 down-regulated lncRNA promoters corresponding to 18 and 27 lncRNAs, respectively. The up-regulated lncRNAs were clustered into two groups, early and late up-regulated groups, which were predicted to associate with the immune activation and the immune response to infection, respectively. Further, the Ingenuity IPA analysis predicted canonical pathways and upstream transcription regulators associated with differentially expressed lncRNAs. Several differentially expressed lncRNAs that have been reported elsewhere revealed various expressional change by M1 or M2 pre-activation and the following MAC infection. Finally, we showed that expressional change of lncRNAs in MAC-infected BMDMs is predominantly mediated by Tlr2, but there may be other weakly sensing mechanism for MAC infection. Taken together, we identified differentially expressed lncRNAs in MAC-infected BMDMs, which revealed diverse features implying their distinct role in MAC infection and macrophage polarization.
2024-01-01 | GSE249460 | GEO
Project description:Rationale: T cell activation is a key antimicrobial component against mycobacterial disease. Programmed cell death-1 (PD-1) and programmed cell death-ligand 1 (PD-L1) pathway could affect the antimicrobial immune responses by suppressing T cell activity. Several recent studies demonstrated that blocking of PD-1/PD-L1 pathway exacerbated Mycobacterium tuberculosis infection. However, the influence of blocking this pathway in pulmonary Mycobacterium avium-intracellulare complex (MAC) infection was not fully understood. Objective: We aimed to determine the influence of genetic depletion of PD-1/PD-L1 pathway on the disease activity of MAC infection. Methods: Wild-type, PD-1-deficient mice and PD-L1-deficient mice were intranasally infected with Mycobacterium avium bacteria. Measurements and Main Results: The depletion of PD-1 or PD-L1 did not affect mortality and bacterial burden in mice infected with MAC. However, remarkable infiltration of CD8 T lymphocytes was observed in the lungs of PD-1 and PD-L1 deficient mice compared to wild-type mice. Comprehensive transcriptome analysis showed that levels of gene expressions related to Th1 immunity did not differ according to the genotypes. However, genes related to the activity of CD8 T cells and related chemokine activity were up-regulated in the infected lungs of PD-1 and PD-L1 deficient mice. Conclusions: Depletion of PD-1/PD-L1 pathway did not affect the activation of Th1 immunity in response to MAC infection, which may explain why MAC infection was controlled in these mice. In addition, CD8-positive T cell pulmonary inflammation in knockout mice might have some clinical implication in the treatment of cancer patients with immune checkpoint inhibitors when the patients are infected with MAC.
2021-09-15 | GSE169202 | GEO
Project description:Aging and the pathophysiology of pulmonary Mycobacterium avium complex (MAC) disease
| PRJNA1213102 | ENA
Project description:Pulmonary Mycobacterium avium complex (MAC) disease shows a range of clinical phenotypes and responses to treatment. While Th1 immunity and neutrophils have been implicated in its pathogenesis, the precise mechanisms remain unclear. Furthermore, comprehensive gene expression analysis in this context are scarce. This study aimed to elucidate the heterogeneity of pulmonary MAC disease by gene expression profiling of whole blood cells. Unsupervised cluster analysis was performed on whole blood gene expression data at 0M. In addition, we also evaluated the variation in gene expression profiles of whole blood cells before (0M) and after starting treatment (1M) with guideline based therapy (GBT; azithromycin [AZM]/clarithromycin [CAM]+ethambutol [EB]+rifampicin [RFP]).
2025-12-08 | GSE288604 | GEO
Project description:We performed scTCR-seq to investigate overall immune cell populations and distribution of MAC-PD patients, according to their clinical outcome.
2024-03-01 | GSE226442 | GEO
Project description:We performed scRNA-seq to investigate overall immune cell populations and distribution of MAC-PD patients, according to their clinical outcome.
2024-03-01 | GSE226099 | GEO
Project description:Transcriptional profiling of primary cutaneous anaplastic large cell lymphoma cell line Mac-1 cells transduced with lenti-virus vector harboring shRNA against SATB1 gene comparing control untreated Mac-1 cells and Mac-1 cells transduced with scrambled shRNA, in which SATB1 expression is not affected. Two condition experiment, SATB1 silenced Mac-1 cells vs control Mac-1 cells. Biological replicates: 2 transduced replicates, 2 control replicates
2013-12-31 | E-GEOD-50916 | biostudies-arrayexpress
Project description:Background: Johne’s disease is a chronic wasting disease caused by the bacterium Mycobacterium avium subspecies paratuberculosis (MAP). Johne’s disease is highly contagious and MAP infection in dairy cattle can eventually lead to death. With no available treatment for Johne’s disease, genetic selection and improvements in management practices could help reduce its prevalence. In a previous study, the gene coding interleukin-10 receptor subunit alpha (IL10Rα) was associated with Johne’s disease in dairy cattle. Our objective was to determine how IL10Rα affects the pathogenesis of MAP by examining the effect of a live MAP challenge on a mammary epithelial cell line (MAC-T) that had IL10Rα knocked out using CRISPR/cas9. The wild type and the IL10Rα knockout MAC-T cell lines were exposed to live MAP bacteria for 48 hours. Thereafter, mRNA was extracted from infected and uninfected cells. Differentially expressed genes were compared between the wild type and the IL10Rα knockout cell lines. Gene ontology was performed based on the differentially expressed genes to determine which biological pathways were involved. Results: Immune system processes pathways were targeted to determine the effect of IL10Rα on the response to MAP infection. There was a difference in immune response between the wild type and IL10Rα knockout MAC-T cell lines, and little difference in immune response between infected and not infected IL10Rα knockout MAC-T cells, indicating IL10Rα plays an important role in the progression of MAP infection. Additionally, these comparisons allowed us to identify other genes involved in inflammation-mediated chemokine and cytokine signalling, interleukin signalling and toll-like receptor pathways. Conclusions: Identifying differentially expressed genes in wild type and ILR10α knockout MAC-T cells infected with live MAP bacteria provided further evidence that IL10Rα contributes to mounting an immune response to MAP infection and allowed us to identify additional potential candidate genes involved in this process. We found there was a complex immune response during MAP infection that is controlled by many genes.
2024-05-20 | GSE247921 | GEO
Project description:Mycobacterium avium subspecies paratuberculosis (MAP) infection is established following the ingestion of bacteria, their penetration of the intestinal mucosa and subsequent events of the host-parasite interaction. These bacteria invade M cells, macrophages and are capable of resisting host defenses and multiply to reach very high numbers intracellular. Mycobactrium avium subsp. avium (MAA) is an antigenically and genetically similar organisms but is relatively nonpathogenic for cattle. MAA organisms appear to infect cattle, but unlike cattle infected with MAP, cattle infected with MAA typically mount an effective systemic immune response, form caseous granuloma, and eliminate the infection. This study was designed to understand the similarities and differences in the host responses during MAP and MAA infection. Neonatal calves were infected (ligated ileal loops) with PBS, MAP, or avirulent MAA following which samples were collected at 30 min, 1h, 2h, 4h, 8h, or 12h. Post-infection, RNA was collected, processed, and then hybridized to custom bovine gene expression arrays, each of which represented 13,258 transcripts spotted in duplicate. Arrays were normalized by scaling against the average reference intensity value (i.e., average across all arrays), normalized by global mean, and then log transformed before statistical analyses were performed. Pairwise comparisons of averaged signal values and Student’s t test were performed using GeneSifter software (VizX Labs, Seattle, WA). A fold-change of at least 1.5-fold and a p value of 0.05 or less was required for a difference in signal to be considered statistically significant. When comparing the transcriptional responses of calves infected with the MAA versus MAP, unique patterns of expression were clearly visible. In general, numbers of transcripts altered in response to infection were much greater for MAA-infected animals than for those infected with the MAP. No genes were significantly up-regulated in MAP-infected animals at the earliest time point tested (30 min), and only modest numbers of genes were increased in expression over the experimental time course. On the other hand, up-regulated transcripts were detected by 30 min in MAA-infected animals and peaked by 2 hr. Differences in the numbers of down-regulated genes between MAP-infected and MAA-infected animals (compared to PBS-infected controls) were less pronounced. At the earliest time points, MAP-infected calves had a greater number of down-regulated genes than did animals infected with MAA. This trend was reversed at 8 and 12 hr post-infection. Keywords: Gene expression profiling by microarray
2012-10-03 | GSE13888 | GEO