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抗生素对细菌诱导的胎膜弱化的抑制作用。

Antibiotic inhibition of bacterially induced fetal membrane weakening.

作者信息

McGregor J A, Schoonmaker J N, Lunt B D, Lawellin D W

机构信息

Department of Obstetrics and Gynecology, University of Colorado Health Sciences Center, Denver.

出版信息

Obstet Gynecol. 1990 Jul;76(1):124-8.

PMID:2193262
Abstract

A fetal membrane model was used to evaluate in vitro the efficacy of two antibiotics, erythromycin and clindamycin, in preventing bacterial protease-induced weakening of amniochorion. Standardized inocula of protease-producing bacteria (10(9) colony-forming units [cfu]/mL Staphylococcus aureus, incubated at 37C for 20 hours) reliably reduced fetal membrane structural integrity as reflected by bursting tension and work to rupture. Supraminimal inhibitory concentrations (supra-MICs) (erythromycin 0.23 microgram/mL; clindamycin 0.56 microgram/mL) and subminimal inhibitory concentrations (sub-MICs) (erythromycin 0.13 microgram/mL; clindamycin 0.06 microgram/mL) of both antibiotics prevented fetal membrane impairment due to test bacteria. Supra-MICs of both antibiotics prevented bacterial cell growth and release of protease. Sub-MICs of both antibiotics allowed bacterial cell growth of test microorganisms but inhibited protease release and subsequent fetal membrane damage. These findings suggest that inhibitory and even subinhibitory doses of antibiotics such as erythromycin and clindamycin may be effective in reducing the occurrence of premature rupture of membranes and subsequent preterm birth mediated by susceptible microorganisms.

摘要

使用胎膜模型在体外评估两种抗生素(红霉素和克林霉素)预防细菌蛋白酶诱导的羊膜绒毛膜弱化的效果。产蛋白酶细菌的标准化接种物(10⁹ 菌落形成单位[cfu]/mL金黄色葡萄球菌,在37℃孵育20小时)可靠地降低了胎膜结构完整性,这通过破裂张力和破裂功来反映。两种抗生素的超最小抑菌浓度(supra - MICs)(红霉素0.23微克/毫升;克林霉素0.56微克/毫升)和亚最小抑菌浓度(sub - MICs)(红霉素0.13微克/毫升;克林霉素0.06微克/毫升)可预防试验细菌导致的胎膜损伤。两种抗生素的supra - MICs可阻止细菌细胞生长和蛋白酶释放。两种抗生素的sub - MICs允许试验微生物的细菌细胞生长,但抑制蛋白酶释放及随后的胎膜损伤。这些发现表明,诸如红霉素和克林霉素等抗生素的抑制剂量甚至亚抑制剂量可能有效减少由易感微生物介导的胎膜早破及随后早产的发生。

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引用本文的文献

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Characterization of the transcriptome of chorioamniotic membranes at the site of rupture in spontaneous labor at term.足月自发性分娩胎膜破裂部位的羊膜转录组特征。
Am J Obstet Gynecol. 2010 May;202(5):462.e1-41. doi: 10.1016/j.ajog.2010.02.045.
2
Pathogenesis to treatment: preventing preterm birth mediated by infection.发病机制与治疗:预防感染介导的早产
Infect Dis Obstet Gynecol. 1997;5(2):106-14. doi: 10.1155/S1064744997000173.
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The role of urogenital tract infections in the etiology of preterm birth: a review.泌尿生殖道感染在早产病因学中的作用:综述
Arch Gynecol Obstet. 1996;258(1):1-19. doi: 10.1007/BF01370927.