ArticlePLoS pathogens2015
IL-1α signaling is critical for leukocyte recruitment after pulmonary Aspergillus fumigatus challenge.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.
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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
104 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.
- Invasive aspergillosis in critically ill patients with diabetes mellitus: a systematic review and meta-analysis.BMC infectious diseases · 2025Pooled it
- Homotypic SLAMF1:SLAMF1 interactions between innate T cells and neutrophils activate fungal killing by neutrophils.bioRxiv : the preprint server for biology · 2026Article
- Cytosolic receptors and signaling in antifungal immunity.The EMBO journal · 2025Review
- An IFN/STAT1/CYBB axis defines protective plasmacytoid DC-neutrophil crosstalk in Aspergillus fumigatus-infected mice.The Journal of clinical investigation · 2025Article
- Aspergillus fumigatus biology, immunopathogenicity and drug resistance.Nature reviews. Microbiology · 2025Review
- Recent developments inMicrobiology and molecular biology reviews : MMBR · 2025Review
- GM-CSF-mediated epithelial-immune cell cross-talk orchestrates pulmonary immunity toScience immunology · 2025Article
- Viral reactivations and fungal infections in nonresolving acute respiratory distress syndrome.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Article
- IFN Receptor 2 Regulates TNF-α-Mediated Damaging Inflammation during Aspergillus Pulmonary Infection.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Epidermal Growth Factor Receptor Signaling Governs the Host Inflammatory Response to Invasive Aspergillosis.bioRxiv : the preprint server for biology · 2024Article
- Epithelial responses to fungal pathogens.Current opinion in microbiology · 2024Review
- Proteome and Dihydrorhodamine Profiling of Bronchoalveolar Lavage in Patients with Chronic Pulmonary Aspergillosis.Journal of fungi (Basel, Switzerland) · 2024Article
- Article
- Pathogenicity and virulence ofVirulence · 2023Review
- Novel Host Pathways Govern Epithelial Cell Invasion of Aspergillus fumigatus.Microbiology spectrum · 2023Article
- Immune responses to human fungal pathogens and therapeutic prospects.Nature reviews. Immunology · 2023Review
- Article
- Immunity to pathogenic fungi in the eye.Seminars in immunology · 2023Review
- Immunity to fungi in the lung.Seminars in immunology · 2023Review
44 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Aspergillus fumigatus is a mold that causes severe pulmonary infections. Our knowledge of how A. fumigatus growth is controlled in the respiratory tract is developing, but still limited. Alveolar macrophages, lung resident macrophages, and airway epithelial cells constitute the first lines of defense against inhaled A. fumigatus conidia. Subsequently, neutrophils and inflammatory CCR2+ monocytes are recruited to the respiratory tract to prevent fungal growth. However, the mechanism of neutrophil and macrophage recruitment to the respiratory tract after A. fumigatus exposure remains an area of ongoing investigation. Here we show that A. fumigatus pulmonary challenge induces expression of the inflammasome-dependent cytokines IL-1β and IL-18 within the first 12 hours, while IL-1α expression continually increases over at least the first 48 hours. Strikingly, Il1r1-deficient mice are highly susceptible to pulmonary A. fumigatus challenge exemplified by robust fungal proliferation in the lung parenchyma. Enhanced susceptibility of Il1r1-deficient mice correlated with defects in leukocyte recruitment and anti-fungal activity. Importantly, IL-1α rather than IL-1β was crucial for optimal leukocyte recruitment. IL-1α signaling enhanced the production of CXCL1. Moreover, CCR2+ monocytes are required for optimal early IL-1α and CXCL1 expression in the lungs, as selective depletion of these cells resulted in their diminished expression, which in turn regulated the early accumulation of neutrophils in the lung after A. fumigatus challenge. Enhancement of pulmonary neutrophil recruitment and anti-fungal activity by CXCL1 treatment could limit fungal growth in the absence of IL-1α signaling. In contrast to the role of IL-1α in neutrophil recruitment, the inflammasome and IL-1β were only essential for optimal activation of anti-fungal activity of macrophages. As such, Pycard-deficient mice are mildly susceptible to A. fumigatus infection. Taken together, our data reveal central, non-redundant roles for IL-1α and IL-1β in controlling A. fumigatus infection in the murine lung.
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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.