Literature DB >> 36008666

Methods Related to the Immunopathogenesis of Vulvovaginal Candidiasis and Associated Neutrophil Anergy.

Junko Yano1, Paul L Fidel2.   

Abstract

Vulvovaginal candidiasis (VVC) is a common mucosal disease, caused primarily by Candida albicans that affects up to 75% of women of childbearing age. The pathogenesis of VVC and recurrent VVC (RVVC) is largely understood after decades of research. In this regard, an immunopathological response involving the migration of neutrophils that become dysfunctional (anergic) in the vaginal environment leads to the symptomatic conditions. However, immunotherapeutic strategies to correct the immunopathogenesis are still elusive. Much of the mechanistic discoveries have been uncovered using the established mouse model of chronic VVC. This chapter details the methods widely used for the mouse model of experimental VVC and associated outcome measures of the immunopathologic response and resulting symptomatic condition and focuses further on assays used to demonstrate "neutrophil anergy" in the model. These methods may serve as a source or resource for further experimentation with the ultimate goal to reduce or eliminate VVC/RVVC.
© 2022. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.

Entities:  

Keywords:  Anergy; Candida albicans; Methods; Mouse model; Neutrophils; Vulvovaginal candidiasis

Mesh:

Year:  2022        PMID: 36008666     DOI: 10.1007/978-1-0716-2549-1_14

Source DB:  PubMed          Journal:  Methods Mol Biol        ISSN: 1064-3745


  9 in total

1.  Major histocompatibility haplotype does not impact the course of experimentally induced murine vaginal candidiasis.

Authors:  C A Black; F M Eyers; M L Dunkley; R L Clancy; K W Beagley
Journal:  Lab Anim Sci       Date:  1999-12

2.  Expression of syndecan-1 in female reproductive tract tissues and cultured keratinocytes.

Authors:  P Inki
Journal:  Mol Hum Reprod       Date:  1997-04       Impact factor: 4.025

Review 3.  Host responses to Candida albicans: Th17 cells and mucosal candidiasis.

Authors:  Heather R Conti; Sarah L Gaffen
Journal:  Microbes Infect       Date:  2010-04-08       Impact factor: 2.700

4.  Hormonal modification of epithelial differentiation and expression of cell surface heparan sulfate proteoglycan in the mouse vaginal epithelium. An immunohistochemical and electron microscopic study.

Authors:  K Hayashi; M Hayashi; E Boutin; G R Cunha; M Bernfield; R L Trelstad
Journal:  Lab Invest       Date:  1988-01       Impact factor: 5.662

5.  Annexin-A1 identified as the oral epithelial cell anti-Candida effector moiety.

Authors:  E A Lilly; J Yano; P L Fidel
Journal:  Mol Oral Microbiol       Date:  2010-08       Impact factor: 3.563

Review 6.  Novel Mechanism behind the Immunopathogenesis of Vulvovaginal Candidiasis: "Neutrophil Anergy".

Authors:  Junko Yano; Brian M Peters; Mairi C Noverr; Paul L Fidel
Journal:  Infect Immun       Date:  2018-02-20       Impact factor: 3.441

7.  The acute neutrophil response mediated by S100 alarmins during vaginal Candida infections is independent of the Th17-pathway.

Authors:  Junko Yano; Jay K Kolls; Kyle I Happel; Floyd Wormley; Karen L Wozniak; Paul L Fidel
Journal:  PLoS One       Date:  2012-09-25       Impact factor: 3.240

8.  Transcriptomic analysis of vulvovaginal candidiasis identifies a role for the NLRP3 inflammasome.

Authors:  Vincent M Bruno; Amol C Shetty; Junko Yano; Paul L Fidel; Mairi C Noverr; Brian M Peters
Journal:  MBio       Date:  2015-04-21       Impact factor: 7.867

9.  Diverse vaginal microbiomes in reproductive-age women with vulvovaginal candidiasis.

Authors:  Mu-Biao Liu; Su-Rong Xu; Yan He; Guan-Hua Deng; Hua-Fang Sheng; Xue-Mei Huang; Cai-Yan Ouyang; Hong-Wei Zhou
Journal:  PLoS One       Date:  2013-11-12       Impact factor: 3.240

  9 in total

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