Fetal skin as a pro-inflammatory organ: Evidence from a primate model of chorioamnionitis.

Intrauterine infection is a primary cause of preterm birth and fetal injury. The pro-inflammatory role of the fetal skin in the setting of intrauterine infection remains poorly characterized. Whether or not inflammation of the fetal skin occurs in primates remains unstudied. Accordingly, we hypothes...

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Main Authors: Suppawat Boonkasidecha, Paranthaman Senthamarai Kannan, Suhas G Kallapur, Alan H Jobe, Matthew W Kemp
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2017-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC5619751?pdf=render
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author Suppawat Boonkasidecha
Paranthaman Senthamarai Kannan
Suhas G Kallapur
Alan H Jobe
Matthew W Kemp
author_facet Suppawat Boonkasidecha
Paranthaman Senthamarai Kannan
Suhas G Kallapur
Alan H Jobe
Matthew W Kemp
author_sort Suppawat Boonkasidecha
collection DOAJ
description Intrauterine infection is a primary cause of preterm birth and fetal injury. The pro-inflammatory role of the fetal skin in the setting of intrauterine infection remains poorly characterized. Whether or not inflammation of the fetal skin occurs in primates remains unstudied. Accordingly, we hypothesized that: i) the fetal primate skin would mount a pro-inflammatory response to preterm birth associated pro-inflammatory agents (lipopolysaccharides from Escherichia coli, live Ureaplasma parvum, interleukin-1β) and; ii) that inhibiting interleukin-1 signaling would decrease the skin inflammatory response.Rhesus macaques with singleton pregnancies received intraamniotic injections of either sterile saline (control) or one of three pro-inflammatory agonists: E. coli lipopolysaccharides, interluekin-1β or live U. parvum under ultrasound guidance. A fourth group of animals received both E. coli lipopolysaccharide and interleukin-1 signaling inhibitor interleukin-1 receptor antagonist (Anakinra) prior to delivery. Animals were surgically delivered at approximately 130 days' gestational age.Intraamniotic lipopolysaccharide caused an inflammatory skin response characterized by increases in interluekin-1β,-6 and -8 mRNA at 16 hours. There was a modest inflammatory response to U. parvum, but interleukin-1β alone caused no inflammatory response in the fetal skin. Intraamniotic Anakinra treatment of lipopolysaccharide-exposed animals significantly reduced skin inflammation.Intraamniotic lipopolysaccharide and U. parvum were associated with modest increases in the expression of inflammatory mediators in primate fetal skin. Although administration of Interleukin-1β alone did not elicit an inflammatory response, lipopolysaccharide-driven skin inflammation was decreased following intraamniotic Anakinra therapy. These findings provide support for the role of the fetal skin in the development of the fetal inflammatory response.
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spelling doaj.art-cdb0fb772a07460ea6c39ead400d98732022-12-21T18:53:04ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01129e018493810.1371/journal.pone.0184938Fetal skin as a pro-inflammatory organ: Evidence from a primate model of chorioamnionitis.Suppawat BoonkasidechaParanthaman Senthamarai KannanSuhas G KallapurAlan H JobeMatthew W KempIntrauterine infection is a primary cause of preterm birth and fetal injury. The pro-inflammatory role of the fetal skin in the setting of intrauterine infection remains poorly characterized. Whether or not inflammation of the fetal skin occurs in primates remains unstudied. Accordingly, we hypothesized that: i) the fetal primate skin would mount a pro-inflammatory response to preterm birth associated pro-inflammatory agents (lipopolysaccharides from Escherichia coli, live Ureaplasma parvum, interleukin-1β) and; ii) that inhibiting interleukin-1 signaling would decrease the skin inflammatory response.Rhesus macaques with singleton pregnancies received intraamniotic injections of either sterile saline (control) or one of three pro-inflammatory agonists: E. coli lipopolysaccharides, interluekin-1β or live U. parvum under ultrasound guidance. A fourth group of animals received both E. coli lipopolysaccharide and interleukin-1 signaling inhibitor interleukin-1 receptor antagonist (Anakinra) prior to delivery. Animals were surgically delivered at approximately 130 days' gestational age.Intraamniotic lipopolysaccharide caused an inflammatory skin response characterized by increases in interluekin-1β,-6 and -8 mRNA at 16 hours. There was a modest inflammatory response to U. parvum, but interleukin-1β alone caused no inflammatory response in the fetal skin. Intraamniotic Anakinra treatment of lipopolysaccharide-exposed animals significantly reduced skin inflammation.Intraamniotic lipopolysaccharide and U. parvum were associated with modest increases in the expression of inflammatory mediators in primate fetal skin. Although administration of Interleukin-1β alone did not elicit an inflammatory response, lipopolysaccharide-driven skin inflammation was decreased following intraamniotic Anakinra therapy. These findings provide support for the role of the fetal skin in the development of the fetal inflammatory response.http://europepmc.org/articles/PMC5619751?pdf=render
spellingShingle Suppawat Boonkasidecha
Paranthaman Senthamarai Kannan
Suhas G Kallapur
Alan H Jobe
Matthew W Kemp
Fetal skin as a pro-inflammatory organ: Evidence from a primate model of chorioamnionitis.
PLoS ONE
title Fetal skin as a pro-inflammatory organ: Evidence from a primate model of chorioamnionitis.
title_full Fetal skin as a pro-inflammatory organ: Evidence from a primate model of chorioamnionitis.
title_fullStr Fetal skin as a pro-inflammatory organ: Evidence from a primate model of chorioamnionitis.
title_full_unstemmed Fetal skin as a pro-inflammatory organ: Evidence from a primate model of chorioamnionitis.
title_short Fetal skin as a pro-inflammatory organ: Evidence from a primate model of chorioamnionitis.
title_sort fetal skin as a pro inflammatory organ evidence from a primate model of chorioamnionitis
url http://europepmc.org/articles/PMC5619751?pdf=render
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AT suhasgkallapur fetalskinasaproinflammatoryorganevidencefromaprimatemodelofchorioamnionitis
AT alanhjobe fetalskinasaproinflammatoryorganevidencefromaprimatemodelofchorioamnionitis
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