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. 2011 Nov;18(11):1128-37.
doi: 10.1177/1933719111408114.

Inflammation of the fetal ovine skin following in utero exposure to Ureaplasma parvum

Matthew W Kemp  1 , Masatoshi Saito, Suhas G Kallapur, Alan H Jobe, Jeffrey A Keelan, Shaofu Li, Boris Kramer, Li Zhang, Christine Knox, Nobuo Yaegashi, John P Newnham
Affiliations

Inflammation of the fetal ovine skin following in utero exposure to Ureaplasma parvum

Matthew W Kemp et al. Reprod Sci. 2011 Nov.

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 1β (IL-1β), IL-6, IL-8, or tumor necrosis factor-α (TNF-α); (2) the fetal skin's response to 7 days of U. parvum exposure is characterized by elevated expression of MCP-1, TNF-α, 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.

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Conflict of interest statement

The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.

Figures

Figure 1.
Figure 1.
Quantitative PCR analysis of cytokine/chemokine expression in cultured primary keratinocytes exposed to 2 × 107 UP in a time-course experiment at 30 minutes, 1, 2, 4, 6, and 8 hours postexposure. Graph represents mean fold change in infected cells ± SEM normalized to uninfected controls (red line). *Statistically significant increase in transcript expression relative to control. PCR polymerase chain reaction; SEM, standard error of the mean; UP, Ureaplasma parvum.
Figure 2.
Figure 2.
Transverse fetal ovine skin sections demonstrating basophilic infiltration of the dermis and epidermis in representative samples taken from control; 7-day UP exposed; or 69-day UP exposed animals. H&E staining of 9 μm frozen sections. Scale bar = 10 μm. Total magnification 400×. H&E indicates hemotoxylin and eosin staining; UP, Ureaplasma parvum.
Figure 3.
Figure 3.
Quantitative PCR analysis of cytokine/chemokine expression in fetal ovine skin exposed UP in utero for either 7 days or 69 days. Bars represent mean fold change (relative to control) ± SEM. *, statistically significant increase in transcript expression relative to control; ⁁, statistically significant difference between 7-day and 69-day UP-exposed tissues. PCR indicates polymerase chain reaction; SEM, standard error of the mean; UP, Ureaplasma parvum.
Figure 4.
Figure 4.
Immunohistochemical analysis of cytokine expression in the fetal skin. Alexa 488 secondary immunofluorescence for IL-1β, IL-8, and TNF-α expression in fetal skin from control, 7-day UP, and 69-day UP exposed animals. UP indicates Ureaplasma parvum
See this image and copyright information in PMC

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