Lactobacillus helveticus HY7801 ameliorates vulvovaginal candidiasis in mice by inhibiting fungal growth and NF-κB activation.

The anti-inflammatory effects of hydrogen peroxide-producing lactic acid bacteria (LAB) against Candida albicans-induced vulvovaginal candidiasis in β-estradiol-immunosuppressed mice were examined. Oral and intravaginal treatment with these LABs significantly decreased the level of viable C. albicans within the vaginal cavity as well as the quantitated myeloperoxidase activity in the vaginal tissues when compared with control untreated mice. Out of all of the LABs tested, Lactobacillus helveticus HY7801 (LH) most potently inhibited vulvovaginal candidiasis. LH also inhibited the expression of the pro-inflammatory cytokines including TNF-α, IL-1β and IL-6, and inflammatory enzymes, COX-2 and iNOS, as well as the activation of NF-κB. However, the addition of LH led to an increase in IL-10 cytokine expression in the vaginal tissues. In addition, the decrease of Lactobacillaceae and the increase of Pasteurellaceae caused by treatment with C. albicans were reversed with oral and intravaginal administration of LH, suggesting a potential shift in the vaginal microflora present. Addition of LH was toxic to C. albicans in vitro when cultured with HeLa cells. Oral administration of LH inhibited lipopolysaccharide (LPS)-induced TNF-α and IL-1β expressions in β-estradiol-immunosuppressed mice but reversed the expression of anti-inflammatory cytokine IL-10 in comparison to levels observed in the normal control group. LH also inhibited the expression of the pro-inflammatory cytokines, TNF-α and IL-1β, and the activation of NF-κB in LPS-stimulated peritoneal macrophages. Based on these findings, LH may ameliorate vulvovaginal candidiasis by suppressing the NF-κB pathway, as well as through inhibition of the growth of C. albicans.