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...

Full description

Saved in:
Bibliographic Details
Published in:International immunopharmacology 2011-11, Vol.11 (11), p.1758-1765
Main Authors: Joo, Hyun-Min, Hyun, Yang-Jin, Myoung, Kil-Sun, Ahn, Young-Tae, Lee, Jung-Hee, Huh, Chul-Sung, Han, Myung Joo, Kim, Dong-Hyun
Format: Article
Language:English
Subjects:
Cell activation
Colony-forming cells
Cyclooxygenase-2
Gardnerella
Gardnerella vaginalis
Hydrogen
Inflammation
Interleukin 10
Interleukin 6
Lactic acid bacteria
Lactobacillus johnsonii
Lipopolysaccharides
Macrophages
Nitric-oxide synthase
Oral administration
Peritoneum
Peroxidase
Vagina
Vaginosis
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1567-5769
DOI:10.1016/j.intimp.2011.07.002