期刊
PLACENTA
卷 28, 期 5-6, 页码 477-481出版社
W B SAUNDERS CO LTD
DOI: 10.1016/j.placenta.2006.08.004
关键词
placenta; toll-like receptor 4; amnion; amniotic epithelium; chorioamnionitis lipopolysaccharide; translocation
资金
- NIAID NIH HHS [K08 AI001759, Y01 AI001759] Funding Source: Medline
- NICHD NIH HHS [HD01264, HD00836, K12 HD001264, K12 HD001264-06] Funding Source: Medline
Toll-like receptor 4 (TLR4) mediates lipopolysaccharide (LPS) induced immune responses, which may contribute to preterm labor associated with intraamniotic gram-negative bacterial infections. The study objective was to investigate gestational age and LPS-induced changes in TLR4 subcellular localization within amniotic epithelium, the first line of host defense against intraamniotic bacteria. TLR4 localization in amniotic epithelium was assessed using immunohistochemistry on 24 placentas of different gestational ages: first trimester (n = 6), second trimester (n = 6), and third trimester (n = 12). Immunofluorescence was used to determine TLR4 localization following ex vivo LPS stimulation of amnion from women undergoing cesarean section without labor at term. TLR4 was expressed in the cytoplasm of amniotic epithelium starting at 9 weeks with apical polarization by 25 weeks gestation. TLR4 localization to the basal membrane was significantly associated with chorioamnionitis (p = 0.01). After LPS stimulation, TLR4 was expressed sequentially within the apical membrane, cytoplasm, and finally in the basal cellular compartment. This suggests that TLR4 expression in amniotic epithelium is poised to monitor amniotic fluid for pathogens. TLR4 translocation to the basal membrane may decrease LPS signaling early in an infection, but allow the amniotic epithelium to remain competent to invasive or intracellular bacteria. (c) 2006 Elsevier Ltd. All rights reserved.
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