Problem: Group B Streptococcus (GBS) is a leading cause of neonatal morbidity and mortality. We tested the hypothesis that the choriodecidua plays a role in GBS-stimulated human beta defensin(HBD)-2 increases in amnion cells through a secreted factor of choriodecidual origin.
Method of study: Human amnion epithelial cells were treated with choriodecidual GBS-conditioned medium, live GBS, lipoteichoic acid (LTA), or lipopolysaccharide (LPS), with and without IL-1 inhibitors.
Results: Choriodecidual tissue punches released IL-1α and IL-1β in response to GBS and this medium significantly stimulated release of HBD-2 by amnion cell cultures. Inhibitors of IL-1 significantly impaired the release of HBD-2 from amnion cells treated with GBS choriodecidual conditioned medium. Direct stimulation of amnion cells with GBS, LTA, or LPS did not increase HBD-2 release.
Conclusion: Paracrine signaling involving IL-1 of choriodecidual origin is likely a critical driver for amnion HBD-2 increases in response to GBS infection of extraplacental membranes.
Keywords: Antimicrobial peptides; extraplacental membranes; group B Streptococcus; human beta defensin; placenta; pregnancy.
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.