Cervical epithelial damage promotes Ureaplasma parvum ascending infection, intrauterine inflammation and preterm birth induction in mice

Pavlidis, Ioannis; Spiller, O. Brad; Demarco, Gabriella Sammut; MacPherson, Heather; Howie, Sarah; Norman, Jane E.; Stock, Sarah

doi:10.1038/s41467-019-14089-y

Cited by 66 publications

(67 citation statements)

References 75 publications

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“…More recently, Pavlidis et al used a mouse model to show ascending infection of Ureaplasma parvum is associated with preterm birth. The study reports an increase in preterm birth from 13% to 28% following vaginal colonisation with Ureaplasma and upregulation of pro-inflammatory cytokines, aligning with the human clinical response 41 . Thus, our data are in accordance with recent literature showing Ureaplasma spp.…”

Section: Microbial Findings In Cervical Culturessupporting

confidence: 55%

Transabdominal amniocentesis in expectant management of preterm premature rupture of membranes: A single center prospective study

Fulova¹,

Hostinská²,

Studničková³

et al. 2021

BIOMED PAP

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The aim of this study was to evaluate the role of IL-6 point-of-care test in amniotic fluid obtained from serial amniocentesis in expectantly managed women with PPROM between 24 and 34 weeks of gestation. Methods. We conducted a prospective observational cohort study which included 62 pregnant women with PPROM in gestational weeks between 22+0 and 34+0. Women aged >18 years were eligible if they presented with PPROM and a singleton pregnancy. Only women who delivered at >24.0 weeks were included in the study. In all women, the maternal blood sampling and a transabdominal amniocentesis were performed at the time of admission prior to the administration of corticosteroids, antibiotics, or tocolytics, to rule out signs of chorioamnionitis. Maternal temperature, maternal serum C-reactive protein (CRP) and white blood cell (WBC) counts were assayed every subsequent day until delivery. Amniotic fluid was used for the clinical assessment (IL-6 point-of-care test, identification of microorganisms in the amniotic fluid. After one week of expectant management of PPROM, second amniocentesis with amniotic fluid sampling was performed in patients who did not deliver. For all newborns, medical records regarding neonatal morbidity and mortality were reviewed. Results. In total, 62 women aged 19 to 41 years were recruited in the study. The mean gestational age at the time of PPROM was 31+0, the mean gestational age at labor was 32+1, and the median time from PPROM to childbirth was 112 h. IL-6 point-of-care test values above 1,000 pg/mL (positive Il-6 AMC) were found in 12 women (19.4%) with median interval from PPROM to childbirth 56 h (min-max: 6.4-288). IL-6 point-of-care test values below 1,000 pg/mL (negative Il-6 AMC) were found in 51 women (81.0%). The neonatal mortality rate was 1.9% and was associated with prematurity. Conclusion. The major clinical finding of our study is that serial transabdominal amniocentesis with Il-6 point-of-care test helps to identify a high inflammatory status in amniotic fluid in women with PPROM. Subsequent expectant management of women with PPROM does not lead to worsening of short-term neonatal outcomes.

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Section: Microbial Findings In Cervical Culturessupporting

confidence: 55%

Transabdominal amniocentesis in expectant management of preterm premature rupture of membranes: A single center prospective study

Fulova¹,

Hostinská²,

Studničková³

et al. 2021

BIOMED PAP

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“…Importantly, both humans and mice have a cervix which forms a tight physical barrier between the vagina and uterine cavity. The cervix plays a critical role in preventing vaginal bacteria from ascending into the uterus (Racicot et al, 2013 ; Pavlidis et al, 2020 ). As in humans, mice have a resident commensal vaginal microbiota and virtually undetectable numbers of microbes in the uterus (Han et al, 2004 ; Digiulio et al, 2010 ).…”

Section: Discussionmentioning

confidence: 99%

A Human Microbiota-Associated Murine Model for Assessing the Impact of the Vaginal Microbiota on Pregnancy Outcomes

Wolfarth

Smith

VanInsberghe

et al. 2020

Front. Cell. Infect. Microbiol.

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Disease states are often linked to large scale changes in microbial community structure that obscure the contributions of individual microbes to disease. Establishing a mechanistic understanding of how microbial community structure contribute to certain diseases, however, remains elusive thereby limiting our ability to develop successful microbiome-based therapeutics. Human microbiota-associated (HMA) mice have emerged as a powerful approach for directly testing the influence of microbial communities on host health and disease, with the transfer of disease phenotypes from humans to germ-free recipient mice widely reported. We developed a HMA mouse model of the human vaginal microbiota to interrogate the effects of Bacterial Vaginosis (BV) on pregnancy outcomes. We collected vaginal swabs from 19 pregnant African American women with and without BV (diagnosed per Nugent score) to colonize female germ-free mice and measure its impact on birth outcomes. There was considerable variability in the microbes that colonized each mouse, with no association to the BV status of the microbiota donor. Although some of the women in the study had adverse birth outcomes, the vaginal microbiota was not predictive of adverse birth outcomes in mice. However, elevated levels of pro-inflammatory cytokines in the uterus of HMA mice were detected during pregnancy. Together, these data outline the potential uses and limitations of HMA mice to elucidate the influence of the vaginal microbiota on health and disease.

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“…Mice were monitored by examining dry tissue placed under the body during anaesthesia recovery 39 . Little leakage was observed.…”

Section: Identification Of Alterations In Gene Expression Induced By mentioning

confidence: 99%

CXCL12 enhances pregnancy outcome via improvement of endometrial receptivity in mice

Koo

Yoon

Hong

et al. 2021

Sci Rep

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Successful pregnancy inevitably depends on the implantation of a competent embryo into a receptive endometrium. Although many substances have been suggested to improve the rate of embryo implantation targeting enhancement of endometrial receptivity, currently there rarely are effective evidence-based treatments to prevent or cure this condition. Here we strongly suggest minimally-invasive intra-uterine administration of embryo-secreted chemokine CXCL12 as an effective therapeutic intervention. Chemokine CXCL12 derived from pre- and peri-implanting embryos significantly enhances the rates of embryo attachment and promoted endothelial vessel formation and sprouting in vitro. Consistently, intra-uterine CXCL12 administration in C57BL/6 mice improved endometrial receptivity showing increased integrin β3 and its ligand osteopontin, and induced endometrial angiogenesis displaying increased numbers of vessel formation near the lining of endometrial epithelial layer with higher CD31 and CD34 expression. Furthermore, intra-uterine CXCL12 application dramatically promoted the rates of embryo implantation with no morphologically retarded embryos. Thus, our present study provides a novel evidence that improved uterine endometrial receptivity and enhanced angiogenesis induced by embryo-derived chemokine CXCL12 may aid to develop a minimally-invasive therapeutic strategy for clinical treatment or supplement for the patients with repeated implantation failure with less risk.

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Cervical epithelial damage promotes Ureaplasma parvum ascending infection, intrauterine inflammation and preterm birth induction in mice

Cited by 66 publications

References 75 publications

Transabdominal amniocentesis in expectant management of preterm premature rupture of membranes: A single center prospective study

Transabdominal amniocentesis in expectant management of preterm premature rupture of membranes: A single center prospective study

A Human Microbiota-Associated Murine Model for Assessing the Impact of the Vaginal Microbiota on Pregnancy Outcomes

CXCL12 enhances pregnancy outcome via improvement of endometrial receptivity in mice

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