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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.

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Mitochondrial STAT3-mediated suppression of apoptosis constrains antimycobacterial immunity

Project description:Maintenance of mitochondrial homeostasis is required to balance the host-pathogen interface during Mycobacterium tuberculosis (Mtb) infection of macrophages. Here, we implicate the non-canonical TRIM family member TRIM14 in regulating mitochondrial health during Mtb infection. Specifically, we show that TRIM14 constrains apoptosis by maintaining a mitochondrial pool of STAT3. TRIM14-dependent mito-STAT3 limits mitochondrial permeability transition pore opening, thereby preserving mitochondrial integrity and raising the threshold for apoptotic commitment. In the absence of TRIM14, increased STAT3 Ser754 phosphorylation reduces mitochondrial STAT3 localization, promoting mPTP opening and apoptosis. In vivo, Trim14 deficiency enhances apoptosis during Mtb infection and is associated with increased CD8+ T cell activation, consistent with apoptotic cell-driven antimycobacterial immunity. Together, these findings define a TRIM14–mito-STAT3 axis that suppresses protective apoptosis during Mtb infection and pinpoint mito-STAT3 as a potential target for host-directed tuberculosis therapies.

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