Bacteria Localization and Chorion Thinning among Preterm Premature Rupture of Membranes

Fortner, Kimberly B.; Grotegut, Chad A.; Ransom, Carla E.; Bentley, Rex C.; Feng, Liping; Lan, Lan; Heine, R. Phillips; Seed, Patrick C.; Murtha, Amy P.

doi:10.1371/journal.pone.0083338

Cited by 67 publications

(50 citation statements)

References 36 publications

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“…The ELGAN studies constituted a large effort that systematically identified bacteria from PTB placentas under this assumption (Olomu et al 2009; Onderdonk et al 2008a,b). However, there is increasing recognition of a large discordance between the presence of bacteria as per culture-based diagnoses and clinical outcome (Watts et al 1992; Pettker et al 2007; Buhimschi et al 2009; Han et al 2009; Leviton et al 2010; Stout et al 2013; Combs et al 2014; Fortner et al 2014). In fact, the presence of placental or membrane bacteria in the absence of histological infection has been discovered repeatedly over the last few decades (Hillier et al 1988; Steel et al 2005; Redline 2007; Stout et al 2013; Fortner et al 2014).…”

Section: The Placental Microbiomementioning

confidence: 99%

The Perinatal Microbiome and Pregnancy: Moving Beyond the Vaginal Microbiome

Prince

Chu

Seferovic

et al. 2015

Cold Spring Harbor Perspectives in Medicine

118

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The human microbiome, the collective genome of the microbial community that is on and within us, has recently been mapped. The initial characterization of healthy subjects has provided investigators with a reference population for interrogating the microbiome in metabolic, intestinal, and reproductive health and disease states. Although it is known that bacteria can colonize the vagina, recent metagenomic studies have shown that the vaginal microbiome varies among reproductive age women. Similarly, the richness and diversity of intestinal microbiota also naturally fluctuate among gravidae in both human and nonhuman primates, as well as mice. Moreover, recent evidence suggests that microbiome niches in pregnancy are not limited to maternal body sites, as the placenta appears to harbor a low biomass microbiome that is presumptively established in early pregnancy and varies in association with a remote history of maternal antenatal infection as well as preterm birth. In this article, we will provide a brief overview on metagenomics science as a means to investigate the microbiome, observations pertaining to both variation and the presumptive potential role of a varied microbiome during pregnancy, and how future studies of the microbiome in pregnancy may lend to a better understanding of human biology, reproductive health, and parturition.

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Section: The Placental Microbiomementioning

confidence: 99%

The Perinatal Microbiome and Pregnancy: Moving Beyond the Vaginal Microbiome

Prince

Chu

Seferovic

et al. 2015

Cold Spring Harbor Perspectives in Medicine

118

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“…Essa situação pode ser o reflexo da utilização de antibióticos no tratamento empírico da sintomatologia genitourinária, sem confirmação laboratorial da colonização. Nesses casos, a antibioterapia erradica as bactérias, mas poderá não ser o suficiente para travar o processo inflamatório subjacente 14,15 . Estudos demonstraram que, apesar da presença de bactérias em 80% das RPM-PT, esta por si só não é suficiente para causar PPT, tendo sido identificada em membranas fetais de grávidas a termo em trabalho de parto ou não 14,15 .…”

Section: Discussionunclassified

“…Nesses casos, a antibioterapia erradica as bactérias, mas poderá não ser o suficiente para travar o processo inflamatório subjacente 14,15 . Estudos demonstraram que, apesar da presença de bactérias em 80% das RPM-PT, esta por si só não é suficiente para causar PPT, tendo sido identificada em membranas fetais de grávidas a termo em trabalho de parto ou não 14,15 . No entanto, demonstramos uma elevação significativa dos parâmetros infecciosos (PCR e leucócitos) no grupo PPTe, reforçando, dessa forma, os dados existentes na literatura 5-7 que apontam para um eventual processo inflamatório sistémico, e não localizado, como um dos potenciais fatores para o desencadear de todo o processo do trabalho de parto pré-termo espontâneo.…”

Section: Discussionunclassified

Parto pré-termo com e sem rotura prematura de membranas: características maternas, obstétricas e neonatais

Brandão¹,

Domingues²,

Fonseca³

et al. 2015

Rev. Bras. Ginecol. Obstet.

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ResumoOBJETIVO: Avaliação das caraterísticas maternas, obstétricas e neonatais nos partos pré-termo (PPT) associados ou não à rotura prematura de membranas pré-termo. MÉTODOS: Estudo retrospetivo de gestações de feto único, com um parto pré-termo, entre 2003 e 2012. Critérios de inclusão: a ocorrência de parto associado ou não à rotura prematura de membranas pré-termo. Critérios de exclusão: partos motivados por comorbidades fetal e/ou maternas (iatrogênicos); e processos não disponíveis ou incompletos para consulta. Foram comparadas caraterísticas entre os dois grupos de PPT: PPT espontâneo (PPTe) versus rotura prematura de membranas pré-termo (RPM-PT), tendo sido utilizados na análise estatística os testes Kolmogorov-Smirnov, Levene, χ ) and higher infectious parameters (Protein C Reactive: 2.2 versus 1.2 mg/L; Leukocytes: 13.3 versus 12.4x10 9 ) were more frequent in PBTs (p<0,001). Neonatal outcomes, specially neurologic outcomes (4.7 versus 2.8%, p<0,001), were worst in PBTs. CONCLUSION: PTB with or without PPROM has a complex etiology. From all evaluated features in our study, only maternal thinness, multiparity with a previous PTB, the cervical length and worst systemic infections parameters were significant in sPTB. This group also showed worst neonatal outcomes, specially on neurological outcomes.

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“…We have previously demonstrated that the quantity of bacteria present in the fetal membranes is correlated with chorion thinning, suggesting that bacterial presence may incrementally evoke a host response that leads to chorion cell death and tissue degradation 94 . There is now evidence that the dose and variation of the MBA of U. parvum might affect the severity of chorioamnionitis in pregnant sheep 95 .…”

Section: Commentmentioning

confidence: 99%

Infection-induced thrombin production: a potential novel mechanism for preterm premature rupture of membranes (PPROM)

Feng

Allen

Marinello

et al. 2018

American Journal of Obstetrics and Gynecology

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Background Preterm premature rupture of membranes (PPROM) is a leading contributor to maternal and neonatal morbidity and mortality. Epidemiologic and experimental studies have demonstrated that thrombin causes fetal membrane weakening and subsequently PPROM. Although blood is suspected as the likely source of thrombin in fetal membranes and amniotic fluid of patients with PPROM, this has not been proven. Ureaplasma Parvum (U. parvum) is emerging as a pathogen involved in prematurity, including PPROM, but until now, prothrombin production directly induced by bacteria in fetal membranes has not been described. Objectives This study was designed to investigate whether U. parvum exposure can induce prothrombin production in fetal membranes cells. Study Design Primary fetal membrane cells (amnion epithelial, chorion trophoblast, and decidua stromal) or full-thickness fetal membrane tissue explants from elective, term, uncomplicated cesarean deliveries were harvested. Cells or tissue explants were infected with live U. parvum (1 × 105, 1 × 106, or 1 × 107 colony forming units (cfu)/ml) or lipopolysaccharide (Escherichia coli J5, L-5014, Sigma, 100 ng/ml or 1000 ng/ml) for 24 hours. Tissue explants were fixed for immunohistochemistry staining of thrombin/prothrombin. Fetal membrane cells were fixed for confocal immunofluorescent staining of the biomarkers of fetal membrane cell types and thrombin/prothrombin. Protein and mRNA were harvested from the cells and tissue explants for Western blot or qRT-PCR to quantify thrombin/prothrombin protein or mRNA production, respectively. Data are presented as mean values ± standard errors of mean. Data were analyzed using one-way ANOVA with post hoc Dunnett’s test. Results Prothrombin production and localization was confirmed by Western blot and immunostainings in all primary fetal membrane cells and tissue explants. Immunofluorescence observations revealed a perinuclear localization of prothrombin in amnion epithelial cells. Localization of prothrombin in chorion and decidua cells was perinuclear and cytoplasmic. Prothrombin mRNA and protein expression in fetal membranes was significantly increased by U. parvum, but not lipopolysaccharide, treatments in a dose-dependent manner. Specifically, U. parvum at a dose of 1×107 cfu/ml significantly increased both prothrombin mRNA (fold changes in amnion: 4.1±1.9; chorion: 5.7±4.2; decidua: 10.0±5.4; FM: 9.2±3.0) and protein expression (fold changes in amnion: 138.0±44.0; chorion: 139.6±15.1; decidua: 56.9±29.1; fetal membrane: 133.1±40.0) compared to untreated controls. U. parvum at a dose of 1×106 cfu/ml significantly upregulated prothrombin protein expression in chorion cells (fold change: 54.9±5.3) and prothrombin mRNA expression in decidua cells (fold change: 4.4±1.9). Conclusions Our results demonstrate that prothrombin can be directly produced by fetal membrane amnion, chorion, and decidua cells. Further, prothrombin production can be stimulated by U. parvum exposure in fetal membranes. These findings represent a potentia...

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Bacteria Localization and Chorion Thinning among Preterm Premature Rupture of Membranes

Cited by 67 publications

References 36 publications

The Perinatal Microbiome and Pregnancy: Moving Beyond the Vaginal Microbiome

The Perinatal Microbiome and Pregnancy: Moving Beyond the Vaginal Microbiome

Parto pré-termo com e sem rotura prematura de membranas: características maternas, obstétricas e neonatais

Infection-induced thrombin production: a potential novel mechanism for preterm premature rupture of membranes (PPROM)

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