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C-Myc Inhibits Macrophage Antimycobacterial Response in Mycobacterium tuberculosis Infection

ABSTRACT: c-Myc Inhibits Macrophage Antimycobacterial Response in Mycobacterium tuberculosis Infection

PROVIDER: PRJNA1271040 | ENA |

REPOSITORIES: ENA

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c-Myc Inhibits Macrophage Antimycobacterial Response in Mycobacterium tuberculosis Infection

Project description:Mycobacterium tuberculosis (MTB) is a major global cause of mortality, responsible for over a million deaths each year. Despite this burden, natural immunity prevents disease in more than 90% of exposed individuals. Previous studies have identified interferon-gamma (IFN-γ) as a key regulator of innate immune defense against MTB. Here, we investigate the impact of IFN-γ timing on macrophage-mediated control of MTB infection. We demonstrate that IFN-γ exposure before infection enhances macrophage antibacterial activity, whereas post-infection exposure does not. Further analysis of this phenotype revealed a strong association between c-Myc signaling and macrophage function in MTB control, as identified through unbiased in vitro systems approaches. Given the difficulty of perturbing c-Myc in primary cells, we developed a lentiviral system for c-Myc inhibition and overexpression. We profiled both datasets (IFN-γ timing and c-Myc inhibition) to characterize the resulting transcriptional shifts.

2025-08-28 | GSE298739 | GEO

Target genes of transcription factor Myc regulated by Mycobacterium tuberculosis EST12

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Macrophage Epithelial Reprogramming Underlies Mycobacterial Granuloma Formation and Promotes Infection

Project description:Mycobacterium tuberculosis infection in humans triggers formation of granulomas, tightly organized immune cell aggregates that are the central structure of tuberculosis. Infected and uninfected macrophages interdigitate, assuming an altered, flattened appearance. Although pathologists have described these changes for over a century, the molecular and cellular programs underlying this transition are unclear. We find that mycobacterial granuloma formation is accompanied by macrophage induction of canonical epithelial molecules and structures. Using the zebrafish-Mycobacterium marinum model, we identify fundamental macrophage reprogramming events that parallel E-cadherin-dependent mesenchymal-epithelial transitions. Macrophage-specific disruption of E-cadherin function results in disordered granuloma formation, enhanced immune cell access, decreased bacterial burden and increased host survival, suggesting that the granuloma can also serve a bacteria-protective role. In humans, we find that granuloma macrophages are similarly transformed. Long considered largely through the prism of immune signaling pathways, granuloma macrophages are reprogrammed by epithelial modules that alter the trajectory of mycobacterial infection.

2016-10-18 | GSE81913 | GEO

Has-miR-30c-1-3p inhibits macrophage autophagy and pro-motes Mycobacterium tuberculosis survival by targeting ATG4B and ATG9B

Project description:Autophagy is a widespread physiological process in the body, which also protects the host by degrading invading pathogens and harmful substances during pathological conditions. However, Mycobacterium tuberculosis (MTB) can affect the process of autophagy by regulating the expres-sion of microRNAs (miRNAs), allowing for immune evasion. In this study, we constructed a model of a strong virulent strain (H37Rv) infection in human macrophage cell line. Following H37Rv infection, we screened 14 differentially expressed miRNAs by RNA-seq and bioinformatics. We predicted and demonstrated that miR-30c-1-3p inhibits autophagy and promotes macrophage survival by targeting ATG4B and ATG9B during the infection process.Additionally, the intervention of miR-30c-1-3p mimics resulted in an increased bacterial load in macrophages, suggesting that MTB achieves immune evasion by upregulating miR-30c-1-3p during infection. In conclusion, our study provides a valuable target for the development of host-directed anti-tuberculosis therapy as well as a new diagnostic marker.

2024-09-06 | GSE276178 | GEO

Expression Analysis of WR99210-treated Mycobacterium tuberculosis H37Rv

Project description:Investigation of whole genome gene expression level changes in Mycobacterium tuberculosis treated with the DHFR inhibitor WR99210, compared to untreated cells. The antimycobacterial properties of WR99210 are further described in Gerum, A., Ulmer, J., Jacobus, D., Jensen, N., Sherman, D., and C. Sibley. 2002. Novel Saccharomyces cerevisiae screen identifies WR99210 analogues that inhibit Mycobacterium tuberculosis dihydrofolate reductase. Antimicrob Agents Chemother 46(11):3362-3369 [PMID:12384337]

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Emodin inhibits macrophage alernative activation

Project description:Emodin inhibits macrophage alernative activation

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Mycobacterium tuberculosis and macrophage response

Project description:Mycobacterium tuberculosis and macrophage response

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Novel Roles of Osteopontin and CXC Chemokine Ligand 7 in the Defense against Mycobacterial Infection

Project description:Granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced human monocyte-derived macrophage (GM-Mphage) or macrophage CSF (M-CSF)-induced human monocyte-derived Mphage (M-Mphage) are distinct in terms of the resistance to Mycobacterium tuberculosis (M. tuberculosis). To elucidate the role of molecules involved in the functional differences between these Mphages, we investigated the gene expression profiles using microarray. After culture of CD14+ monocytes with CSFs, Mphages were cultured with or without BCG (GM-Mf-BCG and M-Mf-BCG). The gene expression profiles from these cells were compared. Chemokines highly expressed in M-Mphages were selected and evaluated for antimycobacterial activity and superoxide production. FN1 and FCGR2B were the most up-regulated genes in GM-Mphage and M-Mphage, respectively. After the stimulation with BCG, 3 chemokine genes (Osteopontin (SPP1), CXC chemokine ligand 7 (CXCL7), and CC chemokine ligand 11 (CCL11)) were highly expressed in M-Mphage-BCG when compared to those in GM-Mf-BCG. A significantly increased resistance to M. tuberculosis H37Ra was observed after the stimulation of GM-Mphage with SPP1 or CXCL7. Superoxide production levels of SPP1- or CXCL7-stimulated GM-Mphages were higher than those of GM-Mphages without stimulation. These results indicate that both SPP1 and CXCL7 might have a role in the resistance against mycobacteria, at least in part, through augmenting reactive oxygen intermediates production in Mphages.

2005-10-05 | GSE3408 | GEO

TraSH analysis of Mycobacterium tuberculosis transposon mutants with reduced bodipy-palmitate uptake on the third day of resting bone marrow-derived macrophage infection

Project description:Mycobacterium tuberculosis transposon mutants with reduced bodipy-palmitate intake on the third day of resting bone marrow-derived macrophage infection are identified by TraSH. Discovery of genetic requirements for fatty acid assimilation by the pathogen is essential for understanding its metabolism during host infection.

2018-11-30 | GSE119753 | GEO

Mycobacterium smegmatis cultured in different carbon sources to induce in vitro cholesterol consumption reveals alterations in immune response after infection: a macrophage proteomics analysis.

Project description:During Tuberculosis, Mycobacterium uses host macrophage cholesterol as a carbon and energy source. To mimic these conditions Mycobacterium smegmatis cultured in minimal medium (MM) has been used to induce cholesterol consumption in vitro. During cultivation, M. smegmatis con-sumes MM cholesterol and changes the accumulation of the cell wall compounds such as PIMs, LM and LAM, which plays an important role in its pathogenicity. These changes led to cell sur-face hydrophobicity modifications and H2O2 susceptibility. Furthermore, when M. smegmatis in-fects J774A.1 macrophages it induces granuloma-like structures formation. The present study aims to access macrophage molecular disturbances caused by M. smegmatis after cholesterol con-sumption through proteomics analyses.

2022-02-17 | PXD025783 | Pride

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