ArticlePLoS pathogens2016
IL-1 Coordinates the Neutrophil Response to C. albicans in the Oral Mucosa.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 116 citations in OpenAlex.
- Beneficial Effect of Olive Leaf Extract as an Adjunct to Standard Antifungal Therapy in TreatingInternational journal of molecular sciences · 2025Trial
- IL-1 family signalling drives mucosal defence against systemic Candida albicans infection.Nature microbiology · 2026Article
- Mussel-inspired coaxial electrospun nanofiber membranes promote scarless oral mucosal repair by enhancing macrophage M2 polarization.Materials today. Bio · 2026Article
- An IL-1, IL-17, and IL-22 cytokine circuit controls vulvovaginal candidiasis independently of estrogen.PLoS pathogens · 2026Article
- Article
- An IFN/STAT1/CYBB axis defines protective plasmacytoid DC-neutrophil crosstalk in Aspergillus fumigatus-infected mice.The Journal of clinical investigation · 2025Article
- IL-1 protects from fatal systemic candidiasis in mice by inhibiting oxidative phosphorylation and hypoxia.Nature communications · 2025Article
- Neutrophil swarming is crucial for limiting oral mucosal infection by Candida albicans.Journal of leukocyte biology · 2025Article
- FHL2 deficiency aggravates Candida albicans infection through decreased myelopoiesis.Science China. Life sciences · 2025Article
- Molecular mechanisms of neutrophil regulatory network in anti-Candida infection.Frontiers in immunology · 2025Review
- Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris.PLoS pathogens · 2024Article
- Unveiling the overlooked fungi: the vital of gut fungi in inflammatory bowel disease and colorectal cancer.Gut pathogens · 2024Review
- Sulfated glycosaminoglycans are host epithelial cell targets of the Candida albicans toxin candidalysin.Nature microbiology · 2024Article
- Immunity to pathogenic mucosal C. albicans infections mediated by oral megakaryocytes activated by IL-17 and candidalysin.Mucosal immunology · 2024Article
- RFX transcription factor in the human-associated yeast Candida albicans regulates adhesion to oral epithelium.Molecular microbiology · 2024Article
- Correlation between salivary cytokine profiles and white spot lesions in adolescent patients receiving clear aligner orthodontic treatment.BMC oral health · 2023Article
- IκBζ is an essential mediator of immunity to oropharyngeal candidiasis.Cell host & microbe · 2023Article
- Neutrophil swarms containing myeloid-derived suppressor cells are crucial for limiting oral mucosal infection by C. albicans.Research square · 2023Article
- NADPH oxidase 2 limits amplification of IL-1β-G-CSF axis and an immature neutrophil subset in murine lung inflammation.Blood advances · 2023Article
- Decoding the host-pathogen interspecies molecular crosstalk during oral candidiasis in humans: anFrontiers in genetics · 2023Article
21 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
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mucosal infections with Candida albicans belong to the most frequent forms of fungal diseases. Host protection is conferred by cellular immunity; however, the induction of antifungal immunity is not well understood. Using a mouse model of oropharyngeal candidiasis (OPC) we show that interleukin-1 receptor (IL-1R) signaling is critical for fungal control at the onset of infection through its impact on neutrophils at two levels. We demonstrate that both the recruitment of circulating neutrophils to the site of infection and the mobilization of newly generated neutrophils from the bone marrow depended on IL-1R. Consistently, IL-1R-deficient mice displayed impaired chemokine production at the site of infection and defective secretion of granulocyte colony-stimulating factor (G-CSF) in the circulation in response to C. albicans. Strikingly, endothelial cells were identified as the primary cellular source of G-CSF during OPC, which responded to IL-1α that was released from keratinocytes in the infected tissue. The IL-1-dependent crosstalk between two different cellular subsets of the nonhematopoietic compartment was confirmed in vitro using a novel murine tongue-derived keratinocyte cell line and an established endothelial cell line. These data establish a new link between IL-1 and granulopoiesis in the context of fungal infection. Together, we identified two complementary mechanisms coordinating the neutrophil response in the oral mucosa, which is critical for preventing fungal growth and dissemination, and thus protects the host from disease.
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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.