Epithelial cell-derived neutrophil-activating peptide-78 is present in fetal membranes and amniotic fluid at increased concentrations with intra-amniotic infection and preterm delivery
Epithelial cell-derived neutrophil-activating peptide-78 is present in fetal membranes and amniotic fluid at increased concentrations with intra-amniotic infection and preterm delivery
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DOI：
10.1095/biolreprod.103.016204
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发表时间：
2004-01-01
影响因子：
3.6
通讯作者：
Mitchell, MD
中科院分区：
文献类型：
--
作者：
Keelan, JA;Yang, J;Mitchell, MD
羊膜内分泌和丰富的上皮细胞衍生的嗜中性粒细胞激活肽（ENA）-78，一个强大的化学引诱剂和激活剂的中性粒细胞，进行了研究，在足月分娩和早产的背景下。ENA-78免疫过氧化物酶染色主要定位于绒毛膜滋养细胞和羊膜上皮在长期和早产的妊娠膜，与较弱和不一致的染色在蜕膜细胞。在羊膜（n = 15）中，随着足月分娩，膜组织匀浆中ENA-78的丰度显著增加（接近4倍），在羊膜和绒毛膜蜕膜（n = 31）中，随着早产，ENA-78的丰度显著增加（接近30倍）。在羊膜组织匀浆提取物中，ENA-78水平与白细胞浸润程度呈正相关（r（2）= 0.481）。在羊水中，无羊膜内感染的早产孕妇的ENA-78中位数水平显著低于感染早产孕妇的ENA-78中位数水平（方差分析P < 0.01）。足月妊娠样品中的水平在分娩前后相似。白细胞介素-1 β和肿瘤坏死因子等均以浓度依赖的方式刺激羊膜单层细胞产生ENA-78。在暴露于脂多糖（5 μ g/ml）2-4小时后，绒毛膜蜕膜外植体产生的ENA-78适度增加。免疫印迹法在绒毛膜蜕膜细胞条件培养液中检测到免疫反应性双联体（类似于8 kDa）。我们的结论是，ENA-78，来自妊娠膜，是目前在羊膜腔中的丰度增加，以应对宫内感染，因此，可能发挥作用的感染驱动的早产和继发于白细胞募集和激活的膜破裂的机制。
Intra-amniotic secretion and abundance of epithelial cell-derived neutrophil-activating peptide (ENA)-78, a potent chemoattractant and activator of neutrophils, was studied in the context of term and preterm parturition. Staining of ENA-78 immunoperoxidase was localized predominantly to chorionic trophoblasts and amniotic epithelium in term and preterm gestational membranes, with weaker and less consistent staining in decidual cells. The abundance of ENA-78 in membrane tissue homogenates was significantly increased (similar to4-fold) with term labor in amnion (n = 15), and with preterm labor (similar to30-fold) in amnion and choriodecidua (n = 31). In amnion tissue homogenate extracts, ENA-78 levels were positively correlated with the degree of leukocyte infiltration (r(2) = 0.481). In amniotic fluids, median ENA-78 levels from pregnancies with preterm labor without intra-amniotic infection were significantly lower (P < 0.01 by ANOVA) than those from pregnancies with preterm deliveries with infection. levels in samples derived from term pregnancies were similar before and after labor. Production of ENA-78 by amnion monolayers was stimulated in a concentration-dependent fashion by both interleukin-1beta and tumor necrosis factor et. Production of ENA-78 by choriodecidual explants was increased modestly after 2-4 h of exposure to lipopolysaccharide (5 mug/ml). An immunoreactive doublet (similar to8 kDa) was detected in choriodecidual explant-conditioned media by immunoblotting. We conclude that ENA-78, derived from the gestational membranes, is present in increased abundance in the amniotic cavity in response to intrauterine infection and, hence, may play a role in the mechanism of infection-driven preterm birth and rupture of membranes secondary to leukocyte recruitment and activation.