Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3417239 | Microbial Pathogenesis | 2008 | 5 Pages |
Abstract
Group B streptococcus (GBS) is one of the leading causes of neonatal infection; however the molecular mechanisms involved are not clearly known. Here we used high and low hemolytic GBS isolates and mutant GBS that lacks β-hemolysin expression and showed that GBS infection or exposure to GBS hemolysin extract induces primary human trophoblast, placental fibroblast and JEG3 trophoblast cell line death, and that GBS-induced trophoblast death was β-hemolysin dependent. The fibroblasts and trophoblasts provide an innate immune barrier between fetal and maternal circulation in the placenta. These data suggest that GBS may disrupt this barrier to invade fetal circulation.
Keywords
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Immunology and Microbiology
Microbiology
Authors
Amber Kaplan, Kathy Chung, Hande Kocak, Cristina Bertolotto, Andy Uh, Calvin J. Hobel, Charles F. Simmons, Kelly Doran, George Y. Liu, Ozlem Equils,