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      Decidual stromal cell-derived PGE 2 regulates macrophage responses to microbial threat

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          Abstract

          Problem:

          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.

          Method of Study:

          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 ( E. coli and Group B Streptococcus (GBS)) was measured in THP-1 cells or primary human placental macrophages. Diclofenac, a nonselective cyclooxygenase inhibitor, and prostaglandin E 2 (PGE 2) 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 co-localization of bacteria and macrophages in vivo and assess PGE 2 production.

          Results:

          In response to LPS, dTHESC and THP-1 co-culture 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 2. In mice with GBS chorioamnionitis, macrophages accumulated at sites of bacterial invasion with increased PGE 2 in amniotic fluid, suggesting such paracrine effects might hold relevance in vivo.

          Conclusion:

          These data suggest key roles for decidual stromal cells in modulating tissue responses to microbial threat through release of PGE 2.

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          Author and article information

          Journal
          8912860
          1403
          Am J Reprod Immunol
          Am. J. Reprod. Immunol.
          American journal of reproductive immunology (New York, N.Y. : 1989)
          1046-7408
          1600-0897
          19 July 2018
          07 August 2018
          October 2018
          01 October 2019
          : 80
          : 4
          : e13032
          Affiliations
          [* ]Division of Infectious Diseases, Department of Medicine, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN
          [§ ]Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN
          []Division of Newborn Medicine, Department of Pediatrics, Washington University School of Medicine, St. Louis, MO
          []The University of the South, Sewanee, TN
          []Department of Obstetrics and Gynecology, Vanderbilt University Medical Center, Nashville, TN
          []Tennessee Valley Healthcare Systems, Department of Veteran Affairs, Nashville, TN
          [# ]Department of Pediatrics, New York University School of Medicine, New York, NY
          [** ]Department of Microbiology, New York University School of Medicine, New York, NY
          Author notes
          Corresponding author: David M. Aronoff, MD, 1161 21 st Avenue South, A-2200 MCN, Nashville, TN 37232-2582, Ph: (615) 322-8972, Fax: (615) 343-6160, d.aronoff@ 123456vanderbilt.edu
          Author information
          http://orcid.org/0000-0003-4587-6121
          Article
          PMC6461368 PMC6461368 6461368 nihpa982180
          10.1111/aji.13032
          6461368
          30084522
          b02aee31-d885-48c3-a915-798be4e676f5
          History
          Categories
          Article

          pregnancy,prostaglandins,infection,chorioamnionitis,fetal membranes,microfluidics

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