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Purinergic, P2X3 positive cells in amniotic membranes

Published:September 29, 2018DOI:https://doi.org/10.1016/j.ajog.2018.09.032
      We congratulate Dr Feng et al on their innovative studies demonstrating infection-induced thrombin production in preterm premature rupture of the membranes (PPROM).
      • Feng L.P.
      • Allen T.K.
      • Marinello W.P.
      • Murtha A.P.
      Infection-induced thrombin production: a potential novel mechanism for preterm, premature, rupture the membranes (PPROM).
      Are similar results demonstrable in vivo using noncultured tissues, and which comes first: the infection or thrombin production? Or does prior denervation of the lower genital tract promote opportunist infection and a diverse cascade of pathologic changes in preterm labor/PPROM?
      • Wu X.Q.
      • Cai Y.Y.
      • Xia W.T.
      • Quinn M.J.
      The aetiology of pre-eclampsia, 1945–1953.
      Our observations in PPROM in simple, rolled membrane preparations demonstrate significant infiltration of both sets of membranes with sheets of inflammatory cells (Figure, A). However, in uncomplicated term pregnancies, we note a layer of cells that express purinergic, P2X3 “stretch” receptors that de-layers in labor (Figure, B and C). We are interested in their relationship to aquaporin (water) channels because aquaporins 1, 3, 8, and 9 are known to be present in membranes;
      • Martínez N.
      • Damiano A.E.
      Aquaporins in fetal development.
      however, it is too early to draw firm conclusions about any associations yet.
      Figure thumbnail gr1
      FigureInflammatory cells, P2X3-positive cells, and de-layering of P2X3-positive layer of cells
      A, Sheets of inflammatory cells obliterate the membranes adjacent to the site of membrane rupture in a rolled membrane preparation (hematoxylin and eosin, magnification, ×200). B, A discrete layer of P2X3-positive cells in maternal chorion after cesarean delivery at term (B) (anti-P2X3, magnification, ×100). C, De-layering of the P2X3-positive layer of cells following spontaneous labor at term (anti-P2X3, magnification, ×100).
      P2X3, P2X purinoceptor 3.
      Zhou. Purinergic, P2X3 positive cells in amniotic membranes. Am J Obstet Gynecol 2019.

      References

        • Feng L.P.
        • Allen T.K.
        • Marinello W.P.
        • Murtha A.P.
        Infection-induced thrombin production: a potential novel mechanism for preterm, premature, rupture the membranes (PPROM).
        AJOG. 2018; 219: 101.e1-101.e12
        • Wu X.Q.
        • Cai Y.Y.
        • Xia W.T.
        • Quinn M.J.
        The aetiology of pre-eclampsia, 1945–1953.
        BJOG. 2016; 123: 2130
        • Martínez N.
        • Damiano A.E.
        Aquaporins in fetal development.
        Adv Exp Med Biol. 2017; 969: 199-212

      Linked Article

      • Infection-induced thrombin production: a potential novel mechanism for preterm premature rupture of membranes (PPROM)
        American Journal of Obstetrics & GynecologyVol. 219Issue 1
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          Preterm premature rupture of membranes is a leading contributor to maternal and neonatal morbidity and death. Epidemiologic and experimental studies have demonstrated that thrombin causes fetal membrane weakening and subsequently preterm premature rupture of membranes. Although blood is suspected to be the likely source of thrombin in fetal membranes and amniotic fluid of patients with preterm premature rupture of membranes, this has not been proved. Ureaplasma parvum is emerging as a pathogen involved in prematurity, which includes preterm premature rupture of membranes; however, until now, prothrombin production that has been induced directly by bacteria in fetal membranes has not been described.
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        American Journal of Obstetrics & GynecologyVol. 220Issue 1
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          We appreciate the thoughtful comments of Dr Quinn and colleagues regarding our recent article.1 In response to their first question, we demonstrated only the results in vitro cell or tissue explants. The cause-effect is an important question; however, our model is not designed to answer a cause-effect relationship but primarily to show how infection can exaggerate a response with thrombin, a known agent that weakens membranes. Depending on the specific type of underlying pathology, thrombin may come first or in other cases infection may arise first.
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