ArticleNature medicine2015
Activation of HIF-1α and LL-37 by commensal bacteria inhibits Candida albicans colonization.
Article in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 267 papers.
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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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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
267 citing papers in PubMed, 418 citations in OpenAlex.
- Effect of intrapartum azithromycin on early childhood gut mycobiota development: post hoc analysis of a double-blind randomized trial.Nature communications · 2025Trial
- Antifungal therapy improves microbiome dynamics in inflammatory bowel disease.Nature medicine · 2026Observational
- An Integrated Platform for the Comprehensive Analysis of Host-Fungal Interactions in the Murine Tongue.Current protocols · 2026Article
- The gut microbiota directs vitamin A flux to regulate intestinal T cell development.Cell host & microbe · 2026Article
- Review
- Intracellular acidification by microbiota-derived valeric acid facilitates trans-kingdom ecology limiting Candida parapsilosis colonization.Cell host & microbe · 2026Article
- A Keratinocyte-Mast Cell NF-κB2/CXCL2/IL-6 Amplification Loop Enhances Cutaneous Antifungal Defense Against C. albicans.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Oxygen homeostasis: new insight of gut microbiota-host interactions.NPJ biofilms and microbiomes · 2026Review
- Integrated analysis of human-mouse gut microbiota in RSV infection based on machine learning.BMC microbiology · 2026Article
- The mycobiome, virome and archaeome in gastrointestinal cancers: molecular pathogenesis and therapeutic intervention.Molecular cancer · 2026Review
- An IL-17-DUOX2 axis controls gastrointestinal colonization by Candida albicans.Nature communications · 2026Article
- Fungi and colorectal cancer: from dysregulation to clinical translation.Gut pathogens · 2026Review
- LL-37: Biological Mechanisms and Emerging Therapeutic Applications in Intestinal Disease.Immunity, inflammation and disease · 2026Review
- Colonic Engyodontium fungus triggers neutrophil antimicrobial activity to suppress Lactobacillus johnsonii-derived glutamic acid-maintained Tregs.The Journal of clinical investigation · 2026Article
- Streptococcus salivarius CCFM1416 Modulates Oral Immunity via IL-17/IKBζ and Combats Candida albicans Infection.Probiotics and antimicrobial proteins · 2026Article
- Bacterial metabolites induce cell wall remodeling, antifungal resistance, and immune recognition of commensal fungi.Current biology : CB · 2026Article
- Commensal fungus to the rescue of gut injury.Nature microbiology · 2026Article
- Clinical impact of altered gut microbiota and metabolite profiles on mortality in patients with candidemia: a prospective observational pilot cohort study.Annals of clinical microbiology and antimicrobials · 2026Observational
- The hidden cost of antibiotics: microbial dysbiosis-induced SCFA imbalance and its underlying mechanisms.Frontiers in immunology · 2026Review
- Interkingdom microbiome physiology in colorectal cancer: barrier dysfunction, immune-metabolic signaling, and therapeutic resistance.Frontiers in physiology · 2026Review
207 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Candida albicans colonization is required for invasive disease. Unlike humans, adult mice with mature intact gut microbiota are resistant to C. albicans gastrointestinal (GI) colonization, but the factors that promote C. albicans colonization resistance are unknown. Here we demonstrate that commensal anaerobic bacteria-specifically clostridial Firmicutes (clusters IV and XIVa) and Bacteroidetes-are critical for maintaining C. albicans colonization resistance in mice. Using Bacteroides thetaiotamicron as a model organism, we find that hypoxia-inducible factor-1α (HIF-1α), a transcription factor important for activating innate immune effectors, and the antimicrobial peptide LL-37 (CRAMP in mice) are key determinants of C. albicans colonization resistance. Although antibiotic treatment enables C. albicans colonization, pharmacologic activation of colonic Hif1a induces CRAMP expression and results in a significant reduction of C. albicans GI colonization and a 50% decrease in mortality from invasive disease. In the setting of antibiotics, Hif1a and Camp (which encodes CRAMP) are required for B. thetaiotamicron-induced protection against C. albicans colonization of the gut. Thus, modulating C. albicans GI colonization by activation of gut mucosal immune effectors may represent a novel therapeutic approach for preventing invasive fungal disease in humans.
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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.