Taken together, the key findings of the study suggested that CXCR3/CXCR4 double-knockout could act to hinder the progression of VVC, highlighting its promise as a novel therapeutic target in the treatment of VVC.
Like in IL-22 deficiency, IL-18 deficiency was associated with an increased susceptibility to VVC and unbalanced Th17/Treg response, suggesting that IL-18 can regulate both the innate and the adaptive responses to the fungus.
The aim of this study was to assess the efficacy of an oral formulation containing Lactobacillus acidophilus GLA-14, Lactobacillus rhamnosus HN001 and bovine lactoferrin on symptoms and recurrence of VVC as adjuvant therapy to topical clotrimazole.
Ultimately, by employing mouse strains resistant or susceptible to chronic VVC, it was determined that heparan sulfate (HS) in the vaginal environment of susceptible mice serves as a competitive ligand for Mac-1 on PMNs, which effectively renders the PMNs incapable of binding to <i>Candida</i> to initiate killing.
Ultimately, by employing mouse strains resistant or susceptible to chronic VVC, it was determined that heparan sulfate (HS) in the vaginal environment of susceptible mice serves as a competitive ligand for Mac-1 on PMNs, which effectively renders the PMNs incapable of binding to <i>Candida</i> to initiate killing.
The aim of the present study was to investigate the association between Mrr1, adenylyl cyclase-associated protein 1 (Cap1) and multi-drug resistance gene 1 (MDR1), and to assess the mutations in Mrr1 and Cap1 in azole-resistant <i>Candida albicans</i> strains.The study isolated 68 <i>C. albicans</i> strains from patients with vulvovaginal candidiasis.
In a mouse model of vulvovaginal candidiasis (VVC), the fungal burden and the levels of pro-inflammatory cytokines, IL-1β, IL-6 and TNF-α showed a increase on co-infection with <i>S. agalactiae</i>, while the level of TH17 T cells and IL-17 in the cervicovaginal lavage fluid were significantly decreased.Our results indicate that <i>S. agalactiae</i> inhibits <i>C. albicans</i> hyphal development by downregulating the expression of <i>EFG1</i>-Hwp1.The interaction between <i>S. agalactiae</i> and <i>C. albicans</i> may attenuate host vaginal mucosal TH17 immunity and contribute to mucosal colonization by <i>C. albicans</i>.
The aim of the present study was to investigate the association between Mrr1, adenylyl cyclase-associated protein 1 (Cap1) and multi-drug resistance gene 1 (MDR1), and to assess the mutations in Mrr1 and Cap1 in azole-resistant <i>Candida albicans</i> strains.The study isolated 68 <i>C. albicans</i> strains from patients with vulvovaginal candidiasis.
VT-1161 is a novel, oral, selective inhibitor of fungal lanosterol demethylase and is being developed for the treatment of recurrent vulvovaginal candidiasis.
Given that vaginal fluids from patients with recurrent VVC had higher levels of IL-9, these findings, by providing novel insights into the pathogenesis of VVC, may pave the way for alternative therapeutic strategies based on IL-9 neutralization.
We investigated the prevalence of vulvovaginal candidiasis due to C. africana in an STD clinic in India and analysed the genetic relatedness of these C. africana isolates with those outside India.
We investigated the prevalence of vulvovaginal candidiasis due to C. africana in an STD clinic in India and analysed the genetic relatedness of these C. africana isolates with those outside India.
These data suggest that the vaginal S100 alarmin response to Candida does not require the cells or cytokines of the Th17 lineage, and therefore, the immunopathogenic inflammatory response during VVC occurs independently of the Th17-pathway.
These data suggest that the vaginal S100 alarmin response to Candida does not require the cells or cytokines of the Th17 lineage, and therefore, the immunopathogenic inflammatory response during VVC occurs independently of the Th17-pathway.