Inflammation of the Fetal Ovine Skin Following in utero Exposure to Ureaplasma parvum

Matthew W. Kemp*, Masatoshi Saito, Suhas G. Kallapur, Alan H. Jobe, Jeffrey A. Keelan, Shaofu Li, Boris Kramer, Li Zhang, Christine L. Knox, Nobuo Yaegashi, John P. Newnham

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

There is increasing evidence linking in utero infection and inflammation to preterm birth. Many commensal urogenital tract microorganisms, including the Mycoplasmas and Ureaplasmas, are commonly detected in association with preterm birth. Using an ovine model of sterile fetal inflammation, we demonstrated previously that the fetal skin generates a robust inflammatory response following in utero exposure to lipopolysaccharides from Escherichia coli. The fetal skin's response to colonization of the amniotic fluid by viable microorganisms remains unstudied. We hypothesised that in utero infection with Ureaplasma parvum serovar 3 would induce a proinflammatory response in the fetal skin. We found that (1) cultured fetal keratinocytes (the primary cellular constituent of the epidermis) respond to U. parvum exposure in vitro by increasing the expression of the chemotactant monocyte chemoattractant protein 1 (MCP-1) but not interleukin 1 beta (IL-1 beta), IL-6, IL-8, or tumor necrosis factor-alpha (TNF-alpha); (2) the fetal skin's response to 7 days of U. parvum exposure is characterized by elevated expression of MCP-1, TNF-alpha, and IL-10; and (3) the magnitude of inflammatory cytokine/chemokine expression in the fetal skin is dependent on the duration of U parvum exposure. These novel findings provide further support for the role of the fetal skin in the development of fetal inflammation and the preterm birth that may follow.
Original languageEnglish
Pages (from-to)1128-1137
JournalReproductive Sciences
Volume18
Issue number11
DOIs
Publication statusPublished - Nov 2011

Keywords

  • preterm birth
  • uterine infection
  • inflammation

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