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- Title
Amniotic Fluid Soluble Myeloid Differentiation-2 ( sMD-2) as Regulator of Intra-amniotic Inflammation in Infection-induced Preterm Birth.
- Authors
Dulay, Antonette T.; Buhimschi, Catalin S.; Zhao, Guomao; Oliver, Emily A.; Abdel ‐ Razeq, Sonya S.; Shook, Lydia L.; Bahtiyar, Mert O.; Buhimschi, Irina A.
- Abstract
Problem TLR4 mediates host responses to pathogens through a mechanism that involves protein myeloid differentiation-2 ( MD-2) and its soluble form sMD-2. The role of sMD2 in intra-amniotic inflammation-induced preterm birth has not been previously explored. Method of study Human amniotic fluid ( AF) sMD-2 was studied by Western blotting in 152 AF samples of patients who had an amniocentesis to rule-out infection (yes infection, n = 50; no infection, n = 50) or women with normal pregnancy outcome (second trimester genetic karyotyping, n = 26; third trimester lung maturity testing, n = 26). Histological localization and mRNA expression of MD2 in fetal membranes were studied by immunohistochemistry and RT- PCR. The ability of fetal membrane to release sMD-2 and inflammatory cytokines was studied in vitro. Results Human AF contains three sMD-2 proteoforms whose levels of expression were lower at term. Intra-amniotic infection upregulated sMD-2. MD-2 mRNA and immunohistochemistry findings concurred. In vitro, LPS and monensin increased, while cycloheximide decreased sMD-2 production. Recombinant sMD-2 modulated TNF-α and IL-6 levels in a dose- and time-dependent fashion. Conclusion sMD2 proteoforms are constitutively present in human AF. The intensity of the intra-amniotic inflammatory response to bacteria or perhaps to other TLR4 ligands may be facilitated through synthesis and release of sMD2 by the amniochorion.
- Subjects
AMNIOTIC liquid; INTERLEUKIN-6; ADAPTOR proteins; AMNIOCENTESIS; PREMATURE labor; IMMUNOHISTOCHEMISTRY; MESSENGER RNA
- Publication
American Journal of Reproductive Immunology, 2015, Vol 73, Issue 6, p507
- ISSN
1046-7408
- Publication type
Article
- DOI
10.1111/aji.12362