ArticleFrontiers in immunology2025
Immunomodulation by bacterial products promotes innate signatures favorable to macrophage responses in tuberculosis infection.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed.
- PulmonaromFrontiers in cellular and infection microbiology · 2026Article
- Trained immunity in cancer and autoimmunity: a double-edged sword in immune memory reprogramming.Frontiers in immunology · 2026Review
- Cell-mediated immune responses of beta-glucan on the pathogenesis of chronic tuberculosis infection.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Tuberculosis remains a leading cause of death from infectious diseases globally, underscoring the need to boost innate responses in monocytes and macrophages to enhance early control of Mycobacterium tuberculosis infection. Trained immunity, a form of innate immune memory, enhances macrophage responsiveness through epigenet ic and metabolic reprogramming, offering a promising approach to strengthen host defenses against M. tuberculosis. Methods: This study evaluated the immunomodulatory potential of pharmaceutical-grade bacterial suspension (BS) and bacterial lysates (BL) in human monocyte-derived macrophages (MDM) and their role in innate response to M. tuberculosis infection. MDMs were stimulated with M. bovis BCG, BS, and BL following a training protocol described for BCG-dependent trained immunity. Results: We observed that BS and BL induced sustained cytokine responses and a metabolic transcriptional profile upon secondary stimulation with M. tuberculosis. BS and BL promoted increased IL-1b production in M. tuberculosis-infected MDMs. Additionally, the expression of surface markers shifted to high levels of CD80, CD86, HLA-DR, TLR2, and CD16 and low expression of CD163, TLR9, CCR2, and TLR4, consistent with an M1 phenotype. Moreover, BS and BL upregulated antimicrobial transcriptional signatures, including autophagy-related MAP1LC3 and ATG16L1. Discussion: These findings indicate that BS and BL engage training-associated transcriptional and phenotypic changes, providing new adjunctive strategies to boost innate responses in tuberculosis and other chronic infections.
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