Bacteria and inflammatory cells in fetal membranes do not always cause preterm labor

被引:239
作者
Steel, JH
Malatos, S
Kennea, N
Edwards, AD
Miles, L
Duggan, P
Reynolds, PR
Feldman, RG
Sullivan, MHF
机构
[1] Inst Reprod & Dev Biol, Dept Obstet & Gynaecol, Wolfson & Weston Res Ctr Family Hlth, London W12 0NN, England
[2] Hammersmith Hosp, MRC Clin Sci Ctr, Imperial Coll London, London W12 0NN, England
[3] Vmax Ltd, Wokingham RG41 5TU, Berks, England
基金
英国医学研究理事会;
关键词
D O I
10.1203/01.PDR.0000153869.96337.90
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Intrauterine infection has been frequently linked with preterm labor before 30 wk of human pregnancy. Many different species of organisms have been detected, leading to the suggestion that infection-induced preterm labor is a generic inflammatory response to organisms rather than a specific response to a limited number of pathogens. The detection of organisms by microbiological culture is a laborious and unreliable process, so the aim of this study was to harness modern molecular techniques to detect organisms in tissues from human pregnancy. A DNA probe specific for conserved regions of bacterial 16S ribosomal RNA sequence was designed and labeled with fluorescein for fluorescence in situ hybridization. Organisms were detected in the great majority (>80%) of fetal membranes after prolonged premature rupture of the fetal membranes and after preterm labor, which was consistent with previous data. Organisms were also detected in fetal membranes after preterm delivery without labor and in term deliveries (with or without tabour). Inflammatory cells were found frequently in the amnion or chorion of preterm fetal membranes but not in term tissues. Our primary finding is that fluorescence in situ hybridization is an appropriate method to detect organisms in human fetal membranes. In addition, our data show that bacteria may be present in fetal membranes without necessarily causing an inflammatory response, so the mere presence of bacteria may not be sufficient to cause preterm labor.
引用
收藏
页码:404 / 411
页数:8
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