In:
American Journal of Reproductive Immunology, Wiley, Vol. 71, No. 1 ( 2014-01), p. 61-72
Abstract:
Infection of human fetal membranes elicits secretion of pro‐inflammatory modulators through its innate immune capacities. We investigated the effect of lipopolysacharide ( LPS ) and progesterone ( P 4) upon expression of TLR ‐4/ M y D 88, TNF α, IL ‐6, IL ‐8, IL ‐10, and HBD 2 on the human amniotic epithelium. Method of study Explants of the human amniotic epithelium were pre‐treated with 0.01, 0.1, and 1.0 μ m of P 4; then cotreated with 1000 ng/mL LPS . TLR ‐4 was immuno‐detected, and concentrations of M y D 88, TNF α, IL ‐6, IL ‐8, IL ‐10, and HBD 2 were quantified by ELISA . Results P 4 significantly reduced the expression of LPS ‐induced TLR ‐4/ M y D 88. LPS increased the concentrations of TNF α, IL ‐6, IL ‐8, IL ‐10, and HBD 2 by factors of 30‐, eight, three, three, and fivefold, respectively. P4 at 1.0 μ m was the most effective dose to blunt the secretion of TNF α, IL ‐6, and HBD ‐2. RU ‐486 blocks the effect of P 4. Conclusion P4 inhibited LPS ‐induced TLR ‐4/ M y D 88 and pro‐inflammatory factors in the human amniotic epithelium. These results could explain partially how P 4 can protect the amniotic region of fetal membranes and generate a compensatory mechanism that limits the secretion of pro‐inflammatory modulators, which could jeopardize the immune privilege during pregnancy.
Type of Medium:
Online Resource
ISSN:
1046-7408
,
1600-0897
DOI:
10.1111/aji.2013.71.issue-1
Language:
English
Publisher:
Wiley
Publication Date:
2014
detail.hit.zdb_id:
2024667-5
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