Lactic acid in the vaginal milieu modulates the Candida-host interaction
Vulvovaginal candidiasis (VVC) is one of the most common infections caused by Candida albicans. VVC is characterized by an inadequate hyperinflammatory response and clinical symptoms associated with Candida colonization of the vaginal mucosa. Compared to other host niches in which C. albicans can ca...
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| Language: | English |
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Taylor & Francis Group
2025-12-01
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| Series: | Virulence |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/21505594.2025.2451165 |
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| author | Diletta Rosati Marisa Valentine Mariolina Bruno Arnab Pradhan Axel Dietschmann Martin Jaeger Ian Leaves Frank L. van de Veerdonk Leo A.B. Joosten Sumita Roy Mark H. T. Stappers Neil A.R. Gow Bernhard Hube Alistair J.P. Brown Mark S. Gresnigt Mihai G. Netea |
| author_facet | Diletta Rosati Marisa Valentine Mariolina Bruno Arnab Pradhan Axel Dietschmann Martin Jaeger Ian Leaves Frank L. van de Veerdonk Leo A.B. Joosten Sumita Roy Mark H. T. Stappers Neil A.R. Gow Bernhard Hube Alistair J.P. Brown Mark S. Gresnigt Mihai G. Netea |
| author_sort | Diletta Rosati |
| collection | DOAJ |
| description | Vulvovaginal candidiasis (VVC) is one of the most common infections caused by Candida albicans. VVC is characterized by an inadequate hyperinflammatory response and clinical symptoms associated with Candida colonization of the vaginal mucosa. Compared to other host niches in which C. albicans can cause infection, the vaginal environment is extremely rich in lactic acid that is produced by the vaginal microbiota. We examined how lactic acid abundance in the vaginal niche impacts the interaction between C. albicans and the human immune system using an in vitro culture in vaginal simulative medium (VSM). The presence of lactic acid in VSM (VSM+LA) increased C. albicans proliferation, hyphal length, and its ability to cause damage during subsequent infection of vaginal epithelial cells. The cell wall of C. albicans cells grown in VSM+LA displayed a robust mannan fibrillar structure, β-glucan exposure, and low chitin content. These cell wall changes were associated with altered immune responses and an increased ability of the fungus to induce trained immunity. Neutrophils were compromised in clearing C. albicans grown in VSM+LA conditions, despite mounting stronger oxidative responses. Collectively, we found that fungal adaptation to lactic acid in a vaginal simulative context increases its immunogenicity favouring a pro-inflammatory state. This potentially contributes to the immune response dysregulation and neutrophil recruitment observed during recurrent VVC. |
| format | Article |
| id | doaj-art-29e05b7674a54307b3cbe793e47ec589 |
| institution | Kabale University |
| issn | 2150-5594 2150-5608 |
| language | English |
| publishDate | 2025-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Virulence |
| spelling | doaj-art-29e05b7674a54307b3cbe793e47ec5892025-01-23T04:05:07ZengTaylor & Francis GroupVirulence2150-55942150-56082025-12-0116110.1080/21505594.2025.2451165Lactic acid in the vaginal milieu modulates the Candida-host interactionDiletta Rosati0Marisa Valentine1Mariolina Bruno2Arnab Pradhan3Axel Dietschmann4Martin Jaeger5Ian Leaves6Frank L. van de Veerdonk7Leo A.B. Joosten8Sumita Roy9Mark H. T. Stappers10Neil A.R. Gow11Bernhard Hube12Alistair J.P. Brown13Mark S. Gresnigt14Mihai G. Netea15Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, T he NetherlandsDepartment of Microbial Pathogenicity Mechanisms, Leibniz Institute for Natural Product Research and Infection Biology - Hans-Knöll-Institute, Jena, GermanyDepartment of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, T he NetherlandsMedical Research Council Centre for Medical Mycology, University of Exeter, Exeter, UKJunior Research Group Adaptive Pathogenicity Strategies, Leibniz Institute for Natural Product Research and Infection Biology - Hans-Knöll-Institute, Jena, GermanyDepartment of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, T he NetherlandsMedical Research Council Centre for Medical Mycology, University of Exeter, Exeter, UKDepartment of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, T he NetherlandsDepartment of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, T he NetherlandsMedical Research Council Centre for Medical Mycology, University of Exeter, Exeter, UKMedical Research Council Centre for Medical Mycology, University of Exeter, Exeter, UKMedical Research Council Centre for Medical Mycology, University of Exeter, Exeter, UKDepartment of Microbial Pathogenicity Mechanisms, Leibniz Institute for Natural Product Research and Infection Biology - Hans-Knöll-Institute, Jena, GermanyMedical Research Council Centre for Medical Mycology, University of Exeter, Exeter, UKJunior Research Group Adaptive Pathogenicity Strategies, Leibniz Institute for Natural Product Research and Infection Biology - Hans-Knöll-Institute, Jena, GermanyDepartment of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, T he NetherlandsVulvovaginal candidiasis (VVC) is one of the most common infections caused by Candida albicans. VVC is characterized by an inadequate hyperinflammatory response and clinical symptoms associated with Candida colonization of the vaginal mucosa. Compared to other host niches in which C. albicans can cause infection, the vaginal environment is extremely rich in lactic acid that is produced by the vaginal microbiota. We examined how lactic acid abundance in the vaginal niche impacts the interaction between C. albicans and the human immune system using an in vitro culture in vaginal simulative medium (VSM). The presence of lactic acid in VSM (VSM+LA) increased C. albicans proliferation, hyphal length, and its ability to cause damage during subsequent infection of vaginal epithelial cells. The cell wall of C. albicans cells grown in VSM+LA displayed a robust mannan fibrillar structure, β-glucan exposure, and low chitin content. These cell wall changes were associated with altered immune responses and an increased ability of the fungus to induce trained immunity. Neutrophils were compromised in clearing C. albicans grown in VSM+LA conditions, despite mounting stronger oxidative responses. Collectively, we found that fungal adaptation to lactic acid in a vaginal simulative context increases its immunogenicity favouring a pro-inflammatory state. This potentially contributes to the immune response dysregulation and neutrophil recruitment observed during recurrent VVC.https://www.tandfonline.com/doi/10.1080/21505594.2025.2451165Vulvovaginal candidiasiscandida albicanshost responselactic acidvaginal simulative medium |
| spellingShingle | Diletta Rosati Marisa Valentine Mariolina Bruno Arnab Pradhan Axel Dietschmann Martin Jaeger Ian Leaves Frank L. van de Veerdonk Leo A.B. Joosten Sumita Roy Mark H. T. Stappers Neil A.R. Gow Bernhard Hube Alistair J.P. Brown Mark S. Gresnigt Mihai G. Netea Lactic acid in the vaginal milieu modulates the Candida-host interaction Virulence Vulvovaginal candidiasis candida albicans host response lactic acid vaginal simulative medium |
| title | Lactic acid in the vaginal milieu modulates the Candida-host interaction |
| title_full | Lactic acid in the vaginal milieu modulates the Candida-host interaction |
| title_fullStr | Lactic acid in the vaginal milieu modulates the Candida-host interaction |
| title_full_unstemmed | Lactic acid in the vaginal milieu modulates the Candida-host interaction |
| title_short | Lactic acid in the vaginal milieu modulates the Candida-host interaction |
| title_sort | lactic acid in the vaginal milieu modulates the candida host interaction |
| topic | Vulvovaginal candidiasis candida albicans host response lactic acid vaginal simulative medium |
| url | https://www.tandfonline.com/doi/10.1080/21505594.2025.2451165 |
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