ArticleCell communication and signaling : CCS2020
TRAF1 suppresses antifungal immunity through CXCL1-mediated neutrophil recruitment during Candida albicans intradermal infection.
Article in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Comparative Analysis of Virulence Traits and Fluconazole-Response Mechanisms in Clinical Isolates ofMicroorganisms · 2026Article
- Evaluation of immunological and gene expression responses induced by Galectin-3 and whole-sonicatedOpen veterinary journal · 2026Article
- EditingBiomolecules · 2026Review
- Relationship Between Virulence Factor Activities, Cytotoxicity ofDentistry journal · 2025Article
- Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024Review
- Differential skin immune responses in mice intradermally infected withMicrobiology spectrum · 2023Article
- From environmental adaptation to host survival: Attributes that mediate pathogenicity ofVirulence · 2022Article
- A Fun-Guide to Innate Immune Responses to Fungal Infections.Journal of fungi (Basel, Switzerland) · 2022Review
- Integrin Regulators in Neutrophils.Cells · 2022Review
- The impact of the Fungus-Host-Microbiota interplay upon Candida albicans infections: current knowledge and new perspectives.FEMS microbiology reviews · 2021Review
- CRISPR-Based Genetic Manipulation ofFrontiers in genome editing · 2020Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCandida albicans is the most common opportunistic human fungal pathogen. The chemokine ligand CXCL1 plays a protective role in fungal infection through the recruitment of neutrophils. TRAF1 (tumor necrosis factor-associated factor 1) can be highly induced by proinflammatory stimuli such as LPS and TNF and has been implicated in septic shock. However, the role of TRAF1 in infection, especially fungal infection, remains elusive. Herein, we reveal that TRAF1 suppresses the antifungal immune response to Candida albicans intradermal infection through the regulation of CXCL1 induction and neutrophil recruitment.
methodsA mouse model of C. albicans intradermal infection was established. The Traf1
resultsTRAF1-deficient mice demonstrated improved control of Candida albicans intradermal infection, and concomitant increase in neutrophil recruitment and reduction in fungal burden. The chemokine CXCL1 was upregulated in the TRAF1-deficient macrophages treated with heat-killed C. albicans. Mechanistically, TRAF1-deficient macrophages showed increased activation of transcription factor NFκB p65. The human CXCL8 was also highly induced in the TRAF1-deficient human keratinocytes upon TNF stimulation through decreasing the activation of transcription factor STAT1. TRAF1-deficient macrophages played a critical role in containing the C. albicans skin infection in vivo.
conclusionTRAF1-deficient mice can better control fungal infection in the skin, a process attributable to the CXCL-neutrophil axis. Mechanistically, TRAF1 likely regulates CXCL1 expression in both macrophages and keratinocytes through the transcriptional factor NFκB and STAT1, respectively. Our finding offers new insight into the understanding of the immune regulatory mechanisms in host defense against C. albicans infection.
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