Lactobacillus johnsonii HY7042 ameliorates Gardnerella vaginalis-induced vaginosis by killing Gardnerella vaginalis and inhibiting NF-I super(o)B activation

Hydrogen peroxide-producing lactic acid bacteria (LAB) were isolated from women's vaginas and their anti-inflammatory effects against Gardnerella vaginalis-induced vaginosis were examined in I super(2)-estradiol-immunosuppressed mice. Oral and intravaginal treatment with five LABs significantly decreased viable G. vaginalis numbers in vaginal cavities and myeloperoxidase activity in mouse vaginal tissues. Of the LABs examined, Lactobacillus johnsonii HY7042 (LJ) most potently inhibited G. vaginalis-induced vaginosis. This LAB also inhibited the expressions of IL-1I super(2), IL-6, TNF-I+/-, COX-2, and iNOS, and the activation of NF-I super(o)B in vaginal tissues, but increased IL-10 expression. Orally administered LJ (0.2 x 10 super(8 CFU/mouse) also inhibited the expression of TNF-I+/- by 91.7% in I) super(2)estradiol-immunosuppressed mice intraperitoneally injected with LPS. However, it increased IL-10 expression by 63.3% in these mice. Furthermore, LJ inhibited the expressions of the pro-inflammatory cytokines, TNF-I+/- and IL-1I super(2), and the activation of NF-I super(o)B in lipopolysaccharide-stimulated peritoneal macrophages. LJ also killed G. vaginalis attached with and without HeLa cells. These findings suggest that LJ inhibits bacterial vaginosis by inhibiting the expressions of COX-2, iNOS, IL-1I super(2), and TNF-I+/- by regulating NF-I super(o)B activation and by killing G. vaginalis, and that LJ could ameliorate bacterial vaginosis.