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Role of Cytokine Signaling in Group B Streptococcus ‐Stimulated Expression of Human Beta Defensin‐2 in Human Extraplacental Membranes
Author(s) -
Boldenow Erica,
Hogan Kelly A.,
Chames Mark C.,
Aronoff David M.,
Xi Chuanwu,
LochCaruso Rita
Publication year - 2015
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12325
Subject(s) - beta defensin , cytokine , defensin , beta (programming language) , group b , signal transduction , streptococcus , microbiology and biotechnology , biology , group a , group (periodic table) , membrane , immunology , chemistry , medicine , bacteria , genetics , computer science , antimicrobial , organic chemistry , programming language
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.
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