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Berlin Brandenburg

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  • 1
    In: American Journal of Reproductive Immunology, October 2018, Vol.80(4), pp.n/a-n/a
    Description: Bacterial chorioamnionitis causes adverse pregnancy outcomes, yet host-microbial interactions are not well characterized within gestational membranes. The decidua, the outermost region of the membranes, is a potential point of entry for bacteria ascending from the vagina to cause chorioamnionitis. We sought to determine whether paracrine communication between decidual stromal cells and macrophages shaped immune responses to microbial sensing. Decidual cell-macrophage interactions were modeled in vitro utilizing decidualized, telomerase-immortalized human endometrial stromal cells (dTHESCs) and phorbol ester-differentiated THP-1 macrophage-like cells. The production of inflammatory mediators in response to LPS was monitored by ELISA for both cell types, while phagocytosis of bacterial pathogens (Escherichia coli and Group B Streptococcus (GBS)) was measured in THP-1 cells or primary human placental macrophages. Diclofenac, a non-selective cyclooxygenase inhibitor, and prostaglandin E (PGE ) were utilized to interrogate prostaglandins as decidual cell-derived paracrine immunomodulators. A mouse model of ascending chorioamnionitis caused by GBS was utilized to assess the colocalization of bacteria and macrophages in vivo and assess PGE production. In response to LPS, dTHESC and THP-1 coculture demonstrated enhancement of most inflammatory mediators, but a potent suppression of macrophage TNF-α generation was observed. This appeared to reflect a paracrine-mediated effect of decidual cell-derived PGE . In mice with GBS chorioamnionitis, macrophages accumulated at sites of bacterial invasion with increased PGE in amniotic fluid, suggesting such paracrine effects might hold relevance in vivo. These data suggest key roles for decidual stromal cells in modulating tissue responses to microbial threat through release of PGE .
    Keywords: Chorioamnionitis ; Fetal Membranes ; Infection ; Microfluidics ; Pregnancy ; Prostaglandins
    ISSN: 1046-7408
    E-ISSN: 1600-0897
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  • 2
    In: American Journal of Reproductive Immunology, March 2017, Vol.77(3), pp.n/a-n/a
    Description: Chorioamnionitis is an acute inflammation of the gestational (extraplacental) membranes, most commonly caused by ascending microbial infection. It is associated with adverse neonatal outcomes including preterm birth, neonatal sepsis, and cerebral palsy. The decidua is the outermost layer of the gestational membranes and is likely an important initial site of contact with microbes during ascending infection. However, little is known about how decidual stromal cells (s) respond to microbial threat. Defining the contributions of individual cell types to the complex medley of inflammatory signals during chorioamnionitis could lead to improved interventions aimed at halting this disease. We review available published data supporting the role for s in responding to microbial infection, with a special focus on their expression of pattern recognition receptors and evidence of their responsiveness to pathogen sensing. While s likely play an important role in sensing and responding to infection during the pathogenesis of chorioamnionitis, important knowledge gaps and areas for future research are highlighted.
    Keywords: Chorioamnionitis ; Decidual Stromal Cells ; Infection ; Microbes ; Pathogen Recognition
    ISSN: 1046-7408
    E-ISSN: 1600-0897
    Library Location Call Number Volume/Issue/Year Availability
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