期刊
REPRODUCTIVE SCIENCES
卷 18, 期 11, 页码 1092-1102出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/1933719111404609
关键词
fetal inflammatory response syndrome; prematurity; innate immunity; IL-1 receptor antagonist
资金
- NIH [HD57869, HL97064]
We tested the hypothesis that interleukin 1 (IL-1) mediates intra-amniotic lipopolysaccharide (LPS)-induced chorioamnionitis in pretermfetal sheep. Time-mated Merino ewes with singleton fetuses received IL-1 alpha, LPS, or saline (control) by intra-amniotic injection 1 to 2 days before operative delivery at 124 +/- 1 days gestational age (N = 5-9/group; term =d 150 days). Recombinant human IL-1 receptor antagonist (rhIL-1ra) was given into the amniotic fluid 3 hours before intra-amniotic LPS or saline to block IL-1 signaling. Inflammation in the chorioamnion was determined by histology, cytokine messenger RNA (mRNA), protein expression, and by quantitation of activated inflammatory cells. Intra-amniotic IL-1 and LPS both induced chorioamnionitis. However, IL-1 blockade with IL-1ra did not decrease intra-amniotic LPS-induced increases in pro-inflammatory cytokine mRNAs, numbers of inflammatory cells, myeloperoxidase, or monocyte chemotactic protein-1-expressing cells in the chorioamnion. We conclude that IL-1 and LPS both can cause chorioamnionitis, but IL-1 is not an important mediator of LPS-induced chorioamnionitis in fetal sheep.
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