ArticlePLoS pathogens2012
Chemokine receptor Ccr1 drives neutrophil-mediated kidney immunopathology and mortality in invasive candidiasis.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 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
90 citing papers in PubMed, 114 citations in OpenAlex.
- Berberine as a Promising Antifungal Agent: Insights into Molecular Mechanisms and Therapeutic Potential.ACS omega · 2026Review
- Chemokine Landscapes of the Tumor Microenvironment.bioRxiv : the preprint server for biology · 2026Article
- In Vivo Evaluation of a Nanoemulsion-Delivered Chromium(III)-Triazole Complex Against Fluconazole-ResistantJournal of fungi (Basel, Switzerland) · 2026Article
- In Murine Disseminated Candidiasis, Serum Amyloid P Component Inhibits Inflammation and C-Reactive Protein Potentiates Inflammation.Pathogens (Basel, Switzerland) · 2026Article
- Expression of Human CEACAM Receptors Promotes Inflammation and Organ Damage During SystemicCells · 2026Article
- GPR43 in eosinophils suppresses the emergence of pathogenic Siglec-FNature communications · 2025Article
- A CARD9 deficiency mouse model recapitulates human chronic CNS candidiasis identifying defective monocytic cell responses in immunopathogenesis.JCI insight · 2025Article
- Lipid droplets restrict phagosome formation in antifungal immunity.Cellular & molecular immunology · 2025Article
- AIM2 enhances Candida albicans infection through promoting macrophage apoptosis via AKT signaling.Cellular and molecular life sciences : CMLS · 2024Article
- Invasive candidiasis.Nature reviews. Disease primers · 2024Review
- TRIM26 alleviates fatal immunopathology by regulating inflammatory neutrophil infiltration during Candida infection.PLoS pathogens · 2024Article
- Isolation of Mouse Neutrophils.Current protocols · 2023Article
- Inflammatory ER stress responses dictate the immunopathogenic progression of systemic candidiasis.The Journal of clinical investigation · 2023Article
- Immune responses to human fungal pathogens and therapeutic prospects.Nature reviews. Immunology · 2023Review
- Exploiting antifungal immunity in the clinical context.Seminars in immunology · 2023Review
- The Protective Role of Interleukin 17A in Acinetobacter baumannii Pneumonia Is Associated with Candida albicans in the Airway.Infection and immunity · 2023Article
- From environmental adaptation to host survival: Attributes that mediate pathogenicity ofVirulence · 2022Article
- Pathogenesis and virulence ofVirulence · 2022Review
- Host immune responses in the central nervous system during fungal infections.Immunological reviews · 2022Review
- IL-23 signaling prevents ferroptosis-driven renal immunopathology during candidiasis.Nature communications · 2022Article
30 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
10 authors at 2 institutions in 1 country.
Funding
Abstract
Invasive candidiasis is the 4(th) leading cause of nosocomial bloodstream infection in the US with mortality that exceeds 40% despite administration of antifungal therapy; neutropenia is a major risk factor for poor outcome after invasive candidiasis. In a fatal mouse model of invasive candidiasis that mimics human bloodstream-derived invasive candidiasis, the most highly infected organ is the kidney and neutrophils are the major cellular mediators of host defense; however, factors regulating neutrophil recruitment have not been previously defined. Here we show that mice lacking chemokine receptor Ccr1, which is widely expressed on leukocytes, had selectively impaired accumulation of neutrophils in the kidney limited to the late phase of the time course of the model; surprisingly, this was associated with improved renal function and survival without affecting tissue fungal burden. Consistent with this, neutrophils from wild-type mice in blood and kidney switched from Ccr1(lo) to Ccr1(high) at late time-points post-infection, when Ccr1 ligands were produced at high levels in the kidney and were chemotactic for kidney neutrophils ex vivo. Further, when a 1∶1 mixture of Ccr1(+/+) and Ccr1(-/-) donor neutrophils was adoptively transferred intravenously into Candida-infected Ccr1(+/+) recipient mice, neutrophil trafficking into the kidney was significantly skewed toward Ccr1(+/+) cells. Thus, neutrophil Ccr1 amplifies late renal immunopathology and increases mortality in invasive candidiasis by mediating excessive recruitment of neutrophils from the blood to the target organ.
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Registered trials
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.