ArticleNature communications2023
Macrophage internalization creates a multidrug-tolerant fungal persister reservoir and facilitates the emergence of drug resistance.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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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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
35 citing papers in PubMed, 53 citations in OpenAlex.
- Immunological fitness of echinocandin-resistantVirulence · 2026Article
- Beyond antifungal susceptibility: molecular mechanisms, detection, and clinical implications of fungal heteroresistance.Molecular biology reports · 2026Review
- Recent Outbreaks, Resistance Trends, and Control Measures inJournal of fungi (Basel, Switzerland) · 2026Review
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- Profound cell wall remodeling inMicrobiology spectrum · 2026Article
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- Echinocandin tolerance and persistencemBio · 2026Article
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- Non-Frontiers in microbiology · 2026Review
- MDM2-P53-V-ATPases axis driven by dehydroevodiamine to fight intracellular bacterial infection.Communications biology · 2025Article
- Persister cells in human fungal pathogens.PLoS pathogens · 2025Review
- Pathogenic Fungal Sensing and Responses to Stressful Host Environments.Annual review of microbiology · 2025Review
- Article
- Antifungal persistence: Clinical relevance and mechanisms.PLoS pathogens · 2025Review
- Article
- Expression of 1,3-β-glucan synthase subunits inAntimicrobial agents and chemotherapy · 2025Article
- Heterogeneity ofMicrobiology spectrum · 2025Article
- Tn-seq screens inmSphere · 2025Article
- Tolerance and heteroresistance to echinocandins inmSphere · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Candida glabrata is a major fungal pathogen notable for causing recalcitrant infections, rapid emergence of drug-resistant strains, and its ability to survive and proliferate within macrophages. Resembling bacterial persisters, a subset of genetically drug-susceptible C. glabrata cells can survive lethal exposure to the fungicidal echinocandin drugs. Herein, we show that macrophage internalization induces cidal drug tolerance in C. glabrata, expanding the persister reservoir from which echinocandin-resistant mutants emerge. We show that this drug tolerance is associated with non-proliferation and is triggered by macrophage-induced oxidative stress, and that deletion of genes involved in reactive oxygen species detoxification significantly increases the emergence of echinocandin-resistant mutants. Finally, we show that the fungicidal drug amphotericin B can kill intracellular C. glabrata echinocandin persisters, reducing emergence of resistance. Our study supports the hypothesis that intra-macrophage C. glabrata is a reservoir of recalcitrant/drug-resistant infections, and that drug alternating strategies can be developed to eliminate this reservoir.
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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.