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Alterations in Syncytiotrophoblast Cytokine Expression Following Treatment with Lipopolysaccharide
Author(s) -
Ma Yuehong,
Mor Gil,
Abrahams Vikki M.,
Buhimschi Irina A,
Buhimschi Catalin S,
Guller Seth
Publication year - 2006
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/j.1600-0897.2005.00347.x
Subject(s) - lipopolysaccharide , cytokine , syncytium , endocrinology , proinflammatory cytokine , syncytiotrophoblast , glucocorticoid , syncytiotrophoblasts , medicine , biology , tumor necrosis factor alpha , immunology , inflammation , placenta , fetus , pregnancy , genetics , human immunodeficiency virus (hiv)
Problem The placental syncytium is a differentiated cell type on the surface of the villus that has the potential to release cytokines directly to maternal blood. Responsiveness of this cell type to inflammatory compounds remains largely unelucidated. Method of study Response to a pro‐inflammatory (lipopolysaccharide, LPS) and an anti‐inflammatory (dexamethasone, DEX) compound was studied in primary cultures of syncytiotrophoblasts (SCTs). Cells were incubated with and without LPS and DEX. Cytokine levels in conditioned media were determined by enzyme‐linked immunosorbent assay and proteome arrays. Results LPS treatment induced a fourfold increase in interleukin‐8 (IL‐8) levels in SCTs. LPS enhanced the expression of both pro‐ and anti‐inflammatory cytokines in SCTs. DEX treatment reduced IL‐8 levels in control and LPS‐treated cultures by 70–90%. Conclusion Cytokine expression in SCTs was enhanced by LPS treatment and this effect was suppressed by glucocorticoid treatment. This suggests that inflammatory compounds may alter cytokine expression in the syncytium throughout gestation.