ArticlePLoS pathogens2008
Mucosal damage and neutropenia are required for Candida albicans dissemination.
Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 207 papers.
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Who cites it
207 citing papers in PubMed, 360 citations in OpenAlex.
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- Dangerous liaisons: Candidalysin and myeloid cells in candidiasis.PLoS pathogens · 2026Article
- Managing Breakthrough Fungal Infections in Hematologic Patients: Determinants and Practical Management from a Latin American Perspective on Behalf of INFOCUS LATAM-ISHAM Working Group.Microorganisms · 2026Review
- Host-Candida auris interactions in the skin.PLoS pathogens · 2026Review
- A host-adapted commensal fungus from pet store mice drives type 2 immunity and cross-kingdom protection.bioRxiv : the preprint server for biology · 2026Article
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- Coordinated regulation of pH alkalinization by two transcription factors promotes fungal commensalism and pathogenicity.Nature communications · 2025Article
- Commensalism and pathogenesis of Candida albicans at the mucosal interface.Nature reviews. Microbiology · 2025Review
- A CARD9 deficiency mouse model recapitulates human chronic CNS candidiasis identifying defective monocytic cell responses in immunopathogenesis.JCI insight · 2025Article
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- Crosstalk between gut microbiota and cancer chemotherapy: current status and trends.Discover oncology · 2024Article
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147 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Candida albicans fungemia in cancer patients is thought to develop from initial gastrointestinal (GI) colonization with subsequent translocation into the bloodstream after administration of chemotherapy. It is unclear what components of the innate immune system are necessary for preventing C. albicans dissemination from the GI tract, but we have hypothesized that both neutropenia and GI mucosal damage are critical for allowing widespread invasive C. albicans disease. We investigated these parameters in a mouse model of C. albicans GI colonization that led to systemic spread after administration of immunosuppression and mucosal damage. After depleting resident GI intestinal flora with antibiotic treatment and achieving stable GI colonization levels of C. albicans, it was determined that systemic chemotherapy with cyclophosphamide led to 100% mortality, whereas selective neutrophil depletion, macrophage depletion, lymphopenia or GI mucosal disruption alone resulted in no mortality. Selective neutrophil depletion combined with GI mucosal disruption led to disseminated fungal infection and 100% mortality ensued. GI translocation and dissemination by C. albicans was also dependent on the organism's ability to transform from the yeast to the hyphal form. This mouse model of GI colonization and fungemia is useful for studying factors of innate host immunity needed to prevent invasive C. albicans disease as well as identifying virulence factors that are necessary for fungal GI colonization and dissemination. The model may also prove valuable for evaluating therapies to control C. albicans infections.
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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.