ArticleeLife2025
β-Glucan reprograms alveolar macrophages via neutrophil/IFNγ axis in a murine model of lung injury.
Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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
11 citing papers in PubMed.
- An Rv1471-expressing chimpanzee adenovirus vaccine confers protection against tuberculosis by inducing alveolar macrophage trained immunity and polyfunctional T-cell responses.Emerging microbes & infections · 2026Article
- Article
- Maladaptive trained immunity as a hematopoietic stem cell driver of inflammaging.Nature aging · 2026Article
- IFNγ-induced memory in human macrophages is sustained by the durability of cytokine signaling itself.The Journal of experimental medicine · 2026Article
- Tissue context as a determinant of trained innate immunity: a conserved molecular toolkit with divergent functional outputs.Journal of leukocyte biology · 2026Review
- Immune evasion of multidrug-resistant bacteria: insights from lung innate immune cells and targeted therapies.Frontiers in cellular and infection microbiology · 2026Review
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Article
- Trained immunity and related memory responses in lung health and disease.Frontiers in immunology · 2026Review
- Review
- The double-edged nature of trained immunity.eLife · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Alveolar macrophages (AMs) reside in the lower airways and play a crucial role in lung health and response to sterile inflammation and infections. AMs possess remarkable adaptability to different environmental challenges that can persist through their memory capacity (trained immunity). β-Glucan has been characterized as a potent inducer of central trained immunity by reprogramming haematopoietic stem cells in the bone marrow. In the present study, we show that systemic administration of β-glucan in mice induces peripheral trained immunity by reprogramming AMs in the lungs, in a Dectin1-independent manner. We furthermore demonstrate that AM reprogramming at both the transcriptional and metabolic levels exacerbate lung injury following bacterial (lipopolysaccharide) or viral (polyI:C) challenges via a neutrophil/IFN-γ-dependent manner. These findings identify an additional facet of β-glucan in trained immunity involving AM reprogramming and shed light on the potential detrimental effects of trained immunity.
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Registered trials
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