ArticleCommunications biology2025
Human alveolar macrophage response to Mycobacterium tuberculosis: immune characteristics underlying large inter-individual variability.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Restricted MHC-II trafficking inbioRxiv : the preprint server for biology · 2026Article
- Dual human lung models reveal compartment-specific activity of anti-tuberculosis drugs and host-directed therapies.Microbiology spectrum · 2026Article
- TGFβ primes alveolar-like macrophages to induce type I IFN following TLR2 activation.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Human iPSC-derived alveolar macrophages reveal macrophage subtype functions of itaconate in M. tuberculosis defense.JCI insight · 2026Article
- Repeated pulmonary dosing of β-glucan-chitosan-PLGA nanoparticles controlsAntimicrobial agents and chemotherapy · 2026Article
- Metabolic reprogramming of macrophages during mycobacterial infection: a review of immunometabolic crosstalk and pathogen manipulation.Frontiers in cellular and infection microbiology · 2026Review
- Deciphering tuberculosis pathway mechanisms via graph neural networks and multimodal deep learning: a comprehensive AI-driven framework for precision medicine.Frontiers in pharmacology · 2026Article
- Human alveolar macrophage function is impaired in tuberculosis contacts with diabetes.EBioMedicine · 2025Article
- NR4A nuclear receptor expression in human macrophages mediates apoptosis and controls Mycobacterium tuberculosis growth.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- B cells inhibit IL-1 family cytokine production and Mycobacterium tuberculosis growth in human CD14+ cells.ImmunoHorizons · 2025Article
- Peptide-Based Strategies AgainstPharmaceuticals (Basel, Switzerland) · 2025Review
- Genes required forbioRxiv : the preprint server for biology · 2025Article
- Spatial transcriptomic analysis of HIV and tuberculosis coinfection in a humanized mouse model reveals unique transcription patterns, immune responses and early morphological alterations.bioRxiv : the preprint server for biology · 2025Article
- Cross-species transcriptomics translation reveals a role for the unfolded protein response in Mycobacterium tuberculosis infection.NPJ systems biology and applications · 2025Article
- Mycobacteria Exploit Host GPR84 to Dampen Pro-Inflammatory Responses and Promote Infection in Macrophages.Microorganisms · 2025Article
- Article
- New insight into arginine and tryptophan metabolism in macrophage activation during tuberculosis.Frontiers in immunology · 2024Review
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Abstract
Mycobacterium tuberculosis (M.tb) infection infects human alveolar macrophages (HAMs). In freshly isolated HAMs from 28 healthy adults, we observe large inter-individual differences in bacterial uptake and growth, with tenfold variation in M.tb load by 72 h. While M.tb infection triggers expression changes of numerous host mRNAs, we examined which genes are most variably expressed (VE genes) between donors, as potential biomarkers of individual tuberculosis (TB) risk. The HAM RNA transcriptome following infection revealed thousands of differentially expressed (DE) genes and differential secretion of 25/27 proteins. Yet only 324 DE genes represent VE genes detected exclusively among DE genes in infected cells. Of 36 DE genes detected at all time points (2, 24, and 72 h), 14 are VE genes, indicating early emergence of the VE gene profile. 9/27 DE proteins following infection were encoded by VE genes. Systems analysis of VE RNAs identified a top-scoring network anchored by IL1B, involved in TB immune response. Independent M.tb-HAM transcriptome results from a TB-endemic region show significant overlap in DE genes, including VE genes identified in the main study. Thus, we identify a VE gene network activated upon M.tb-HAM infection with high inter-person variability, guiding studies on determining individual risk of M.tb infection and/or disease.
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