ArticleCellular microbiology2018
Competition of Candida glabrata against Lactobacillus is Hog1 dependent.
Article in Cellular microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
The trial behind it
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
17 citing papers in PubMed, 22 citations in OpenAlex.
- Review
- Distinct properties of human pathogenicmSystems · 2026Article
- Biotin synthesis and assimilation are vital for pathobiology of the insect pathogenic fungusMycology · 2026Article
- Uridine diphosphateFEMS microbes · 2026Article
- Increased fungal burden in the gastrointestinal tract of brain-dead organ donors.Microbiology spectrum · 2025Article
- Advancements in vaginal microbiota,Microbial cell (Graz, Austria) · 2025Review
- Article
- Review
- The Hog1 MAPK substrate governs Candida glabrata-epithelial cell adhesion via the histone H2A variant.PLoS genetics · 2024Article
- Oxidative stress response pathways in fungi.Cellular and molecular life sciences : CMLS · 2022Review
- Review
- Human PathogenicJournal of fungi (Basel, Switzerland) · 2020Article
- Article
- Article
- The role of Lactobacillus species in the control of Candida via biotrophic interactions.Microbial cell (Graz, Austria) · 2019Review
- Competition of Candida glabrata against Lactobacillus is Hog1 dependent.Cellular microbiology · 2018Article
- Hog1 Regulates Stress Tolerance and Virulence in the Emerging Fungal Pathogen Candida auris.mSphere · 2018Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Candida glabrata is a common human fungal commensal and opportunistic pathogen. This fungus shows remarkable resilience as it can form recalcitrant biofilms on indwelling catheters, has intrinsic resistance against azole antifungals, and is causing vulvovaginal candidiasis. As a nosocomial pathogen, it can cause life-threatening bloodstream infections in immune-compromised patients. Here, we investigate the potential role of the high osmolarity glycerol response (HOG) MAP kinase pathway for C. glabrata virulence. The C. glabrata MAP kinase CgHog1 becomes activated by a variety of environmental stress conditions such as osmotic stress, low pH, and carboxylic acids and subsequently accumulates in the nucleus. We found that CgHog1 allows C. glabrata to persist within murine macrophages, but it is not required for systemic infection in a mouse model. C. glabrata and Lactobacilli co-colonise mucosal surfaces. Lactic acid at a concentration produced by vaginal Lactobacillus spp. causes CgHog1 phosphorylation and accumulation in the nucleus. In addition, CgHog1 enables C. glabrata to tolerate different Lactobacillus spp. and their metabolites when grown in co-culture. Using a phenotypic diverse set of clinical C. glabrata isolates, we find that the HOG pathway is likely the main quantitative determinant of lactic acid stress resistance. Taken together, our data indicate that CgHog1 has an important role in the confrontation of C. glabrata with the common vaginal flora.
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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.