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Related Experiment Video

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Purification of HLA-G+ Extravillous Trophoblasts from Human Term Placental Tissues for Phenotyping and Functional Analysis
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Toll-like receptor-2 expression in normal and pathologic human placenta.

Erika Rindsjö1, Ulrika Holmlund, Eva Sverremark-Ekström

  • 1Department of Medicine, Clinical Allergy Research Unit, Karolinska University Hospital Solna, SE-171 76 Stockholm, Sweden. erika.rindsjo@ki.se

Human Pathology
|January 24, 2007
PubMed
Summary

Toll-like receptor 2 (TLR2) expression in the placenta is lower with chorioamnionitis. TLR2 levels vary by pregnancy outcome and trimester, suggesting a role in placental infection response.

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Area of Science:

  • Immunology
  • Obstetrics
  • Perinatology

Background:

  • Toll-like receptors (TLRs) are key innate immune system components.
  • TLRs are expressed by placental trophoblast, but their role in pregnancy, especially with infection, is unclear.

Purpose of the Study:

  • To investigate Toll-like receptor 2 (TLR2) expression in placentas from pregnancies complicated by chorioamnionitis and uncomplicated pregnancies.
  • To determine the localization and differential expression of TLR2 in relation to pregnancy outcomes and gestational age.

Main Methods:

  • Immunohistochemistry was employed to analyze TLR2 expression.
  • Placental tissues were examined from 58 cases of second/third-trimester chorioamnionitis and 25 uncomplicated full-term pregnancies.

Main Results:

  • TLR2 was localized to trophoblast cells and decidual stromal cells.
  • Placentas with chorioamnionitis showed significantly lower TLR2 expression compared to uncomplicated cases.
  • Higher TLR2 expression was observed in placentas from liveborn infants versus stillborn/aborted fetuses.
  • TLR2 expression was higher in second-trimester placentas than in third-trimester placentas.

Conclusions:

  • Reduced TLR2 expression in the placenta may be associated with chorioamnionitis.
  • TLR2 expression in trophoblast cells potentially plays a role in the placental response to infectious pathogens.