Research Topic

Vulvovaginal candidiasis: Unraveling Fungal and Host Mechanisms that Drive Immunopathology

About this Research Topic

Vaginal candidiasis (VVC) is a common disorder in women of childbearing age, caused primarily by Candida albicans. Since C. albicans is a commensal fungus of the vaginal mucosa, a long-standing question remains as to how the fungus switches from harmless commensal to pathogen. Clinical studies and murine vaginitis models suggest that host inflammatory processes drive the onset of symptomatic infection. However, overgrowth of Candida, equipped with an arsenal of virulence factors, is not always obviously correlated with symptomatic VVC. Similarly, fungal burden alone is not predictive of disease.

During VVC, C. albicans undergoes the yeast to hyphae transition, forms biofilms, expresses adhesins and invasins, produces hydrolytic enzymes and candidalysin that synergize to cause epithelial cell damage. The host epithelium and immune system respond by secreting pro-inflammatory cytokines and recruiting large number of non-protective neutrophils. An important area of research aims to define how these virulence attributes, along with host genetic diversity, contribute to human VVC and how are these attributes may differ in recurrent form of VVC (RVVC).

Recruited neutrophils during VVC not only are ineffective against C. albicans, but they are believed to actually exacerbate symptoms. The lack of neutrophil anti-C. albicans activity may be due to heparan sulfate, co-colonizing bacteria, fungal factors or a combination of all three. In particular, different studies suggest that specific inhibitors of neutrophil function are present in the vaginal environment during VVC. The specific nature of these inhibitors is currently a hot topic of VVC pathogenesis studies.

Moreover, fungal cell wall molecules can also induce inflammation through activation of epithelial and immune receptors that trigger pro-inflammatory cytokines and chemokines, but pathogenic fungi can evade recognition by masking these molecules. Knowledge about which cell wall epitopes are available for immune recognition during human infection could implicate specific ligands and receptors in the symptoms of vaginal candidiasis.

The aim of this Research Topic is to focus on recent advances uncovering pathogenicity and host defense evasion mechanisms underpinning the immunopathogenesis of VVC, including genetic and biological aspects of the fungus and the host during their interaction.

Authors are encouraged to contribute original scientific articles including clinical trials, reviews and mini reviews focusing on the following areas:

-Mechanisms of Candida-induced pathogenesis in the vaginal environment
-Mechanisms of host-response to fungal antigens during VVC and RVVC
-Role of host response and fungal biomarkers of VVC onset and\or RVVC persistence
-Mechanisms of anti-fungal drugs or compounds


Keywords: Candida, VVC, pathogenicity, vaginal


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Vaginal candidiasis (VVC) is a common disorder in women of childbearing age, caused primarily by Candida albicans. Since C. albicans is a commensal fungus of the vaginal mucosa, a long-standing question remains as to how the fungus switches from harmless commensal to pathogen. Clinical studies and murine vaginitis models suggest that host inflammatory processes drive the onset of symptomatic infection. However, overgrowth of Candida, equipped with an arsenal of virulence factors, is not always obviously correlated with symptomatic VVC. Similarly, fungal burden alone is not predictive of disease.

During VVC, C. albicans undergoes the yeast to hyphae transition, forms biofilms, expresses adhesins and invasins, produces hydrolytic enzymes and candidalysin that synergize to cause epithelial cell damage. The host epithelium and immune system respond by secreting pro-inflammatory cytokines and recruiting large number of non-protective neutrophils. An important area of research aims to define how these virulence attributes, along with host genetic diversity, contribute to human VVC and how are these attributes may differ in recurrent form of VVC (RVVC).

Recruited neutrophils during VVC not only are ineffective against C. albicans, but they are believed to actually exacerbate symptoms. The lack of neutrophil anti-C. albicans activity may be due to heparan sulfate, co-colonizing bacteria, fungal factors or a combination of all three. In particular, different studies suggest that specific inhibitors of neutrophil function are present in the vaginal environment during VVC. The specific nature of these inhibitors is currently a hot topic of VVC pathogenesis studies.

Moreover, fungal cell wall molecules can also induce inflammation through activation of epithelial and immune receptors that trigger pro-inflammatory cytokines and chemokines, but pathogenic fungi can evade recognition by masking these molecules. Knowledge about which cell wall epitopes are available for immune recognition during human infection could implicate specific ligands and receptors in the symptoms of vaginal candidiasis.

The aim of this Research Topic is to focus on recent advances uncovering pathogenicity and host defense evasion mechanisms underpinning the immunopathogenesis of VVC, including genetic and biological aspects of the fungus and the host during their interaction.

Authors are encouraged to contribute original scientific articles including clinical trials, reviews and mini reviews focusing on the following areas:

-Mechanisms of Candida-induced pathogenesis in the vaginal environment
-Mechanisms of host-response to fungal antigens during VVC and RVVC
-Role of host response and fungal biomarkers of VVC onset and\or RVVC persistence
-Mechanisms of anti-fungal drugs or compounds


Keywords: Candida, VVC, pathogenicity, vaginal


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

07 July 2020 Abstract
04 November 2020 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

07 July 2020 Abstract
04 November 2020 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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