期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 210, 期 6, 页码 1265-1281出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20122753
关键词
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资金
- National Institutes of Health (NIH) [R01AI100989, R01AI070749, K08AI067910]
- March of Dimes grant [21-FY08-562, 21-FY06-77]
- NIH [5 T32 HD007233-29, T32 AI07509]
- NLM, NIH
- Cuyamaca Foundation
- [R01AI31871]
Microbial infection of the amniotic fluid is a significant cause of fetal injury, preterm birth, and newborn infections. Group B Streptococcus (GBS) is an important human bacterial pathogen associated with preterm birth, fetal injury, and neonatal mortality. Although GBS has been isolated from amniotic fluid of women in preterm labor, mechanisms of in utero infection remain unknown. Previous studies indicated that GBS are unable to invade human amniotic epithelial cells (hAECs), which represent the last barrier to the amniotic cavity and fetus. We show that GBS invades hAECs and strains lacking the hemolysin repressor CovR/S accelerate amniotic barrier failure and penetrate chorioamniotic membranes in a hemolysin-dependent manner. Clinical GBS isolates obtained from women in preterm labor are hyperhemolytic and some are associated with covR/S mutations. We demonstrate for the first time that hemolytic and cytolytic activity of GBS is due to the ornithine rhamnolipid pigment and not due to a pore-forming protein toxin. Our studies emphasize the importance of the hemolytic GBS pigment in ascending infection and fetal injury.
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