Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0184938
Title: Fetal skin as a pro-inflammatory organ: Evidence from a primate model of chorioamnionitis
Authors: Boonkasidecha, S
Kannan, PS
Kallapur, SG
Jobe, AH
Kemp, MW 
Keywords: Animals
Chorioamnionitis
Disease Models, Animal
Female
Fetus
Inflammation
Inflammation Mediators
Interleukin-1beta
Interleukin-8
Keratins
Lipopolysaccharides
Macaca mulatta
Male
Polymerase Chain Reaction
Pregnancy
RNA, Messenger
Skin
Ureaplasma
Issue Date: 1-Sep-2017
Publisher: Public Library of Science (PLoS)
Citation: Boonkasidecha, S, Kannan, PS, Kallapur, SG, Jobe, AH, Kemp, MW (2017-09-01). Fetal skin as a pro-inflammatory organ: Evidence from a primate model of chorioamnionitis. PLoS ONE 12 (9) : e0184938-. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0184938
Abstract: Background: 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. Methods: 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. Results: 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. Conclusions: 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.
Source Title: PLoS ONE
URI: https://scholarbank.nus.edu.sg/handle/10635/234974
ISSN: 1932-6203
DOI: 10.1371/journal.pone.0184938
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