ArticleCell host & microbe2020
Legionella-Infected Macrophages Engage the Alveolar Epithelium to Metabolically Reprogram Myeloid Cells and Promote Antibacterial Inflammation.
Article in Cell host & microbe, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 75 citations in OpenAlex.
- Gut microbiome-derived propionate reprograms alveolar macrophages metabolically and regulates lung injury responses in mice.Gut microbes · 2026Article
- GM-CSF signaling on monocytes and monocyte-derived dendritic cells is required for effective pulmonary immunity tobioRxiv : the preprint server for biology · 2026Article
- Threat assessment shapes neutrophil cell fate upon inflammasome activation.Science advances · 2026Article
- Alveolar macrophage-neutrophil crosstalk in acute lung injury: mechanisms, feedback loops, and therapeutic opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- GM-CSF orchestrates monocyte and granulocyte responses to Cryptococcus gattii.PLoS pathogens · 2026Article
- Molecular evolution and adaptations ofFrontiers in cellular and infection microbiology · 2026Review
- Impaired immune metabolism in COPD driven by dysfunction of CXCL16 + alveolar macrophages: multivariate causal evidence.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Pathogenicity and virulence ofVirulence · 2025Review
- Neutralizing GM-CSF autoantibodies impair neutrophil antifungal effector function in a patient with aspergillosis.The Journal of infection · 2025Article
- The Brief Case:Journal of clinical microbiology · 2025Review
- Article
- GM-CSF engages multiple signaling pathways to enhance pro-inflammatory cytokine responses in human monocytes duringInfection and immunity · 2025Article
- Targeting alveolar macrophages: a promising intervention for pulmonary infection and acute lung injury.Cellular & molecular biology letters · 2025Review
- Interleukin-1 receptor antagonist is a conserved early factor for exacerbating tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2025Article
- GM-CSF-mediated epithelial-immune cell cross-talk orchestrates pulmonary immunity toScience immunology · 2025Article
- Considering local immunity for innovative immunomodulatory approaches: pulmonary sepsis as a use case.Frontiers in immunology · 2025Review
- Role of toll-like receptors in pulmonary immunity: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Review
- Regional specialization within the mammalian respiratory immune system.Trends in immunology · 2024Review
- The unique Legionella longbeachae capsule favors intracellular replication and immune evasion.PLoS pathogens · 2024Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
Alveolar macrophages are among the first immune cells that respond to inhaled pathogens. However, numerous pathogens block macrophage-intrinsic immune responses, making it unclear how robust antimicrobial responses are generated. The intracellular bacterium Legionella pneumophila inhibits host translation, thereby impairing cytokine production by infected macrophages. Nevertheless, Legionella-infected macrophages induce an interleukin-1 (IL-1)-dependent inflammatory cytokine response by recruited monocytes and other cells that controls infection. How IL-1 directs these cells to produce inflammatory cytokines is unknown. Here, we show that collaboration with the alveolar epithelium is critical for controlling infection. IL-1 induces the alveolar epithelium to produce granulocyte-macrophage colony-stimulating factor (GM-CSF). Intriguingly, GM-CSF signaling amplifies inflammatory cytokine production in recruited monocytes by enhancing Toll-like receptor (TLR)-induced glycolysis. Our findings reveal that alveolar macrophages engage alveolar epithelial signals to metabolically reprogram monocytes for antibacterial inflammation.
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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.