Abstract
Vulvovaginal candidiasis (VVC) is an inflammatory disease of the vagina mainly caused by Candida albicans (C. albicans), which affects around three-quarters of all women during their reproductive age. Although some antifungal drugs such as azoles have been applied clinically for many years, their therapeutic value is very limited due to the emergence of drug-resistant strains. Previous studies have shown that the adhesion of C. albicans to vaginal epithelial cells is essential for the pathogenesis of VVC. Therefore, preventing the adhesion of C. albicans to vaginal epithelial cells may be one of the most effective strategies for the treatment of VVC. Berberine (BBR) is a biologically active herbal alkaloid that was used to treat VVC. However, so far, its mechanism has remained unclear. This study shows BBR significantly inhibits the adhesion of C. albicans to vaginal epithelial cells by reducing the expressions of ICAM-1, mucin1, and mucin4 in vaginal epithelial cells, which play the most important role in modulating the adhesion of C. albicans to host cells, and balancing IL-2 and IL-4 expressions, which play a key effect on regulating the inflammatory response caused by C. albicans infection. Hence, our findings demonstrate that BBR may be a potential therapeutic agent for VVC by interfering with the adhesion of C. albicans to vaginal epithelial cells and represents a new pathway for developing antifungal therapies agents from natural herbs.
Highlights
Candida albicans, a yeast-hypha dimorphic fungus, is widely found in the vagina, gastrointestinal tract, oral cavity, and on skin surface (Richardson et al, 2019), which results in opportunistic infection under certain circumstances and causes diseases such as Vulvovaginal Candidiasis (VVC)
Our results show that BBR significantly inhibits the adhesion of C. albicans to vaginal epithelial cells by decreasing the expression of ICAM-1, mucin1, and mucin4 in cells and balancing IL-2 and IL4 expression during inflammation and shows its potential therapeutic value on VVC
Our results showed that this compound had no effects on the viability of C. albicans at the subinhibitory concentrations of 16 and 32 μg/ml (Figures 1A,B), while it could significantly reduce this fungal viability in a dose and time-dependent manner at concentrations higher than 32 μg/ ml (Figure 1C)
Summary
A yeast-hypha dimorphic fungus, is widely found in the vagina, gastrointestinal tract, oral cavity, and on skin surface (Richardson et al, 2019), which results in opportunistic infection under certain circumstances and causes diseases such as Vulvovaginal Candidiasis (VVC). Studies have shown that C. albicans infection can stimulate vaginal epithelial cells to highly express adhesion molecules, such as ICAM-1, mucin, and mucin (Moncla et al, 2016; Mikamo et al, 2018) These increasingly regulatory molecules can create a favorable microenvironment for the colonization of C. albicans and the following disorders of local immune homeostasis. The inhibition of C. albicans adhesion and the protection of vaginal mucosal epithelial cells may be a potential strategy that prevents the VVC occurrence and development Conventional antifungal drugs, such as fluconazole and echinocandin, mainly target the cell wall or cell membrane, so as to inhibit or even kill fungi, rather than to block fungal adhesion to host cells (Eschenauer, et al, 2015). Our results show that BBR significantly inhibits the adhesion of C. albicans to vaginal epithelial cells by decreasing the expression of ICAM-1, mucin, and mucin in cells and balancing IL-2 and IL4 expression during inflammation and shows its potential therapeutic value on VVC. The characterization of the herbal compound involved in the regulation of adhesion in VVC pathogenesis may lead to novel anti-fungal therapies that could significantly improve treatment for VVC reducing the public health burden of such diseases
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