ArticlePLoS pathogens2022
Control of β-glucan exposure by the endo-1,3-glucanase Eng1 in Candida albicans modulates virulence.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 56 citations in OpenAlex.
- Article
- Infection-induced glucose starvation triggers NINJ1-dependent macrophage lysis and Candida escape.Nature communications · 2026Article
- Human Dectin-1- and Dectin-2-targeted DectiSomes are effective against diverse pathogenic fungi.Antimicrobial agents and chemotherapy · 2026Article
- Loss of Fgr41 inInfection and immunity · 2026Article
- Glycogen phosphorylase L confers metabolic flexibility in neutrophils to fight fungal infections in nutrient-deprived tissues.Cell host & microbe · 2026Article
- Protein-related hydrophobicity differences among strains belonging toMicrobiology spectrum · 2026Article
- Bacterial metabolites induce cell wall remodeling, antifungal resistance, and immune recognition of commensal fungi.Current biology : CB · 2026Article
- The structural language of fungal cell wall sugars in WHO priority fungi: the determinant of pathogenicity and the gateway to new therapies.Frontiers in immunology · 2026Review
- Manganese homeostasis modulates glucan and chitin unmasking in the opportunistic yeastVirulence · 2025Article
- Lactic Acid Influences Iron Assimilation by a Fungal Pathogen via the Iron Reductive Uptake Pathway.MicrobiologyOpen · 2025Article
- Protein kinase A signaling regulates immune evasion by shaving and concealing fungal β-1,3-glucan.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Functional properties ofMicrobiology (Reading, England) · 2025Article
- Article
- Cas5 Regulates the Exposure of β-Glucan, the Cell Surface Hydrophobicity, and the Expression of Cell Wall Proteins to Remodel theMicroorganisms · 2025Article
- The Use of Specific Non-Journal of fungi (Basel, Switzerland) · 2025Article
- β-1,6-Glucan plays a central role in the structure and remodeling of the bilaminate fungal cell wall.eLife · 2024Article
- ThemBio · 2024Article
- Manipulation of host phagocytosis by fungal pathogens and therapeutic opportunities.Nature microbiology · 2024Review
- Alteration of β-glucan in the emerging fungal pathogen Candida auris leads to immune evasion and increased virulence.Medical microbiology and immunology · 2024Article
- Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Candida albicans is a major opportunistic pathogen of humans. It can grow as morphologically distinct yeast, pseudohyphae and hyphae, and the ability to switch reversibly among different forms is critical for its virulence. The relationship between morphogenesis and innate immune recognition is not quite clear. Dectin-1 is a major C-type lectin receptor that recognizes β-glucan in the fungal cell wall. C. albicans β-glucan is usually masked by the outer mannan layer of the cell wall. Whether and how β-glucan masking is differentially regulated during hyphal morphogenesis is not fully understood. Here we show that the endo-1,3-glucanase Eng1 is differentially expressed in yeast, and together with Yeast Wall Protein 1 (Ywp1), regulates β-glucan exposure and Dectin-1-dependent immune activation of macrophage by yeast cells. ENG1 deletion results in enhanced Dectin-1 binding at the septa of yeast cells; while eng1 ywp1 yeast cells show strong overall Dectin-1 binding similar to hyphae of wild-type and eng1 mutants. Correlatively, hyphae of wild-type and eng1 induced similar levels of cytokines in macrophage. ENG1 expression and Eng1-mediated β-glucan trimming are also regulated by antifungal drugs, lactate and N-acetylglucosamine. Deletion of ENG1 modulates virulence in the mouse model of hematogenously disseminated candidiasis in a Dectin-1-dependent manner. The eng1 mutant exhibited attenuated lethality in male mice, but enhanced lethality in female mice, which was associated with a stronger renal immune response and lower fungal burden. Thus, Eng1-regulated β-glucan exposure in yeast cells modulates the balance between immune protection and immunopathogenesis during disseminated candidiasis.
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