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ORIGINAL ARTICLE: IL‐10 Modulates Placental Responses to TLR Ligands
Author(s) -
Bayraktar Mehmet,
Peltier Morgan,
Vetrano Anna,
Arita Yuko,
Gurzenda Ellen,
Joseph Ansamma,
Kazzaz Jeffrey,
Sharma Surendra,
Hanzeeh
Publication year - 2009
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.1600-0897.2009.00756.x
Subject(s) - lipoteichoic acid , lipopolysaccharide , cytokine , monocyte , proinflammatory cytokine , receptor , inflammation , chemistry , immunology , prostaglandin , biology , endocrinology , bacteria , staphylococcus aureus , biochemistry , genetics
Problem Intra‐uterine infections increase production of pro‐inflammatory cytokines. It is unclear whether different infectious agents determine the relative expression of pro‐and anti‐inflammatory cytokines. Methods of study We compared the placental inflammatory response induced by bacterial lipopolysaccharide (LPS, endotoxin from Gram‐negative bacteria) with those induced by lipoteichoic acid (LTA, a cell wall component of Gram‐positive bacteria). Placental explants from term delivery were treated with either LPS or LTA, in the presence or absence of IL‐10, for 24 hrs. Cytokines, prostaglandin E 2 (PGE 2 ) production and cyclo‐oxygenase‐2 (COX‐2) expression were quantified. Results Both LTA and LPS significantly induced several cytokines with LPS eliciting more potent effects. IL‐6 and IL‐8 were induced to comparable levels in response to both LTA and LPS whereas monocyte chemotactic protein‐1 (MCP‐1) production was induced more by LTA, demonstrating a differential placental response to a specific toll‐like receptor (TLR) ligand. IL‐10 treatment significantly reduced most pro‐inflammatory cytokines as well as PGE 2 induced by both LPS and LTA. Interestingly, IL‐10 down‐regulated LTA‐mediated MCP1 induction, but not that mediated by LPS. Moreover, IL‐10 was more effective in down‐regulating PGE 2 after LPS‐ when compared with LTA stimulation. Conclusions Our results demonstrate that placental exposure to LTA and LPS appear to trigger distinct cytokine responses that can be modulated by IL‐10.