ArticleCell host & microbe2015
Myeloid Growth Factors Promote Resistance to Mycobacterial Infection by Curtailing Granuloma Necrosis through Macrophage Replenishment.
Article in Cell host & microbe, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
61 citing papers in PubMed, 118 citations in OpenAlex.
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- Macrophage adaptation to hypoxia in the tuberculous granuloma potentiates mycobacterium-induced mitochondrial damage and granuloma necrosis.bioRxiv : the preprint server for biology · 2026Article
- Immunopathogenesis of Sarcoidosis.Seminars in respiratory and critical care medicine · 2025Review
- Exploring a Rare Association: Systematic Review of Hypercalcemia in Nontuberculous Mycobacterial Infections.Microorganisms · 2025Review
- Necrosis drives susceptibility toInfection and immunity · 2025Article
- Uptake of Biomimetic Nanovesicles by Granuloma for Photodynamic Therapy of Tuberculosis.ACS omega · 2025Article
- 3D Hydrogel Culture System Recapitulates Key Tuberculosis Phenotypes and Demonstrates Pyrazinamide Efficacy.Advanced healthcare materials · 2025Article
- Leveraging insights from cancer to improve tuberculosis therapy.Trends in molecular medicine · 2025Article
- Necrosis drives susceptibility tobioRxiv : the preprint server for biology · 2024Article
- Metagenomic shotgun sequencing reveals the enrichment ofComputational and structural biotechnology journal · 2024Article
- Immune mechanisms of granuloma formation in sarcoidosis and tuberculosis.The Journal of clinical investigation · 2024Review
- Understanding the development of tuberculous granulomas: insights into host protection and pathogenesis, a review in humans and animals.Frontiers in immunology · 2024Review
- Transcriptional profiling of zebrafish identifies host factors controlling susceptibility to Shigella flexneri.Disease models & mechanisms · 2024Article
- Extracellular vesicles in bacterial and fungal diseases - Pathogenesis to diagnostic biomarkers.Virulence · 2023Review
- The Mineralocorticoid Receptor Plays a Crucial Role in Macrophage Development and Function.Endocrinology · 2023Article
- A macrophage subpopulation promotes airineme-mediated intercellular communication in a matrix metalloproteinase-9 dependent manner.Cell reports · 2023Article
- Nanoparticle-based targeting of microglia improves the neural regeneration enhancing effects of immunosuppression in the zebrafish retina.Communications biology · 2023Article
- Role of B Cells in Mycobacterium Tuberculosis Infection.Vaccines · 2023Review
- Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
The mycobacterial ESX-1 virulence locus accelerates macrophage recruitment to the forming tuberculous granuloma. Newly recruited macrophages phagocytose previously infected apoptotic macrophages to become new bacterial growth niches. Granuloma macrophages can then necrose, releasing mycobacteria into the extracellular milieu, which potentiates their growth even further. Using zebrafish with genetic or pharmacologically induced macrophage deficiencies, we find that global macrophage deficits increase susceptibility to mycobacterial infection by accelerating granuloma necrosis. This is because reduction in the macrophage supply below a critical threshold decreases granuloma macrophage replenishment to the point where apoptotic infected macrophages, failing to get engulfed, necrose. Reducing macrophage demand by removing bacterial ESX-1 offsets the susceptibility of macrophage deficits. Conversely, increasing macrophage supply in wild-type fish by overexpressing myeloid growth factors induces resistance by curtailing necrosis. These findings may explain the susceptibility of humans with mononuclear cytopenias to mycobacterial infections and highlight the therapeutic potential of myeloid growth factors in tuberculosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.