Journal
AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
Volume 62, Issue 6, Pages 390-399Publisher
WILEY
DOI: 10.1111/j.1600-0897.2009.00756.x
Keywords
IL-10; inflammation; lipopolysaccharide; lipoteichoic acid; pre-term labor
Categories
Funding
- NCRR NIH HHS [P20 RR018728] Funding Source: Medline
- NIEHS NIH HHS [P42 ES013660] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available