This systematic review and meta-analysis were performed to assess the association between MBL2 codon 54 genotype and vulvovaginal candidiasis (VVC) or recurrent VVC (RVVC).
The presence of VVC can increase vaginal MBL level, which may be an immune response against Candida albicans infection; in women with rVVC, the low level of MBL in the vagina caused by mutation in the MBL gene may play a role in the recurrence of the infection.
Frequency of interleukin-4 (IL-4) -589 gene polymorphism and vaginal concentrations of IL-4, nitric oxide, and mannose-binding lectin in women with recurrent vulvovaginal candidiasis.
This study suggests that PD exerts inhibitory effects on C. albicans proliferation, adhesion and inflammation and simultaneously downregulates the expression levels of important genes and proteins associated with the Dectin-1 pathway, highlighting the potential application of PD to improve the clinical management of VVC.
The analysis of individuals with these mutations demonstrates that dectin-1 is critical for the host defense against vulvovaginal candidiasis and candidal colonization of the gastrointestinal tract.
We describe a family in which four women who were affected by either recurrent vulvovaginal candidiasis or onychomycosis had the early-stop-codon mutation Tyr238X in the beta-glucan receptor dectin-1.
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 unrestrained activation of the NLRP3 inflammasome with continuous production of IL-1β and recruitment of neutrophils is recognized as a pathogenic factor in VVC.
We demonstrate that mice lacking IL-17RA, Act1, or IL-22 showed no evidence for altered VVC susceptibility or immunopathology, regardless of estrogen administration.
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>.
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.
The unrestrained activation of the NLRP3 inflammasome with continuous production of IL-1β and recruitment of neutrophils is recognized as a pathogenic factor in VVC.
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>.
Therefore, we conducted the present study in order to investigate whether microRNA-1192 (miR-1192) would significantly target CXCR4 in Th17 cells as well as inflammatory factors in mouse models suffering from VVC.