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确定临床或亚临床绒毛膜羊膜炎所致早产中母体和胎儿的细胞免疫作用。

Determining the maternal and fetal cellular immunologic contributions in preterm deliveries with clinical or subclinical chorioamnionitis.

作者信息

McNamara M F, Wallis T, Qureshi F, Jacques S M, Gonik B

机构信息

Department of Obstetrics and Gynecology Wayne State University School of Medicine Detroit MI USA.

出版信息

Infect Dis Obstet Gynecol. 1997;5(4):273-9. doi: 10.1155/S1064744997000471.

DOI:10.1155/S1064744997000471
PMID:18476151
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2364556/
Abstract

OBJECTIVE

Our purpose was to determine the maternal and fetal polymorphonuclear contributions to preterm histologic chorioamnionitis and whether this response differs in clinical chorioamnionitis when compared to cases without clinical chorioamnionitis.

METHODS

Paraffin placenta blocks from 19 preterm deliveries with histologic chorioamnionitis, 9 with clinical chorioamnionitis and 10 without clinical chorioamnionitis, were identified. Only placentas from male fetuses were used. Cytospin slides were generated from tissue specimens for fluorescent in situ hybridization (FISH) and labeled with X and Y chromosome probes. Under fluorescent microscopy, polymorphonuclear cells (PMNs) were identified as having two XX signals (maternal) or a single X and Y pair (fetal).

RESULTS

Maternal PMNs comprised 89% and 91% of the cellular response in the groups with and without clinical chorioaminionitis, respectively. This difference in the two groups was not statistically significant.

CONCLUSIONS

The dominant contribution of PMNs seen in preterm severe histologic chorioamnionitis is maternal in origin. This response is similar in the presence or absence of clinical chorioamnionitis.

摘要

目的

我们的目的是确定母体和胎儿多形核细胞对早产组织学绒毛膜羊膜炎的贡献,以及与无临床绒毛膜羊膜炎的病例相比,这种反应在临床绒毛膜羊膜炎中是否存在差异。

方法

识别出19例早产且伴有组织学绒毛膜羊膜炎、9例伴有临床绒毛膜羊膜炎以及10例无临床绒毛膜羊膜炎的石蜡胎盘块。仅使用来自男性胎儿的胎盘。从组织标本制备细胞涂片用于荧光原位杂交(FISH),并用X和Y染色体探针标记。在荧光显微镜下,多形核细胞(PMN)被鉴定为具有两个XX信号(母体)或单个X和Y对(胎儿)。

结果

在有和无临床绒毛膜羊膜炎的组中,母体PMN分别占细胞反应的89%和91%。两组之间的这种差异无统计学意义。

结论

早产严重组织学绒毛膜羊膜炎中所见PMN的主要贡献源自母体。在有或无临床绒毛膜羊膜炎的情况下,这种反应相似。

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