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Am J Obstet Gynecol. 2012 Mar;206(3):208.e1-7. doi: 10.1016/j.ajog.2011.12.036. Epub 2012 Feb 12.

Inflammation promotes a cytokine response and disrupts the cervical epithelial barrier: a possible mechanism of premature cervical remodeling and preterm birth.

Author information

  • 1Maternal and Child Health Research Program, Department of Obstetrics and Gynecology, Center for Research on Reproduction and Women's Health, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA. Christopher.Nold@uphs.upenn.edu

Abstract

OBJECTIVE:

An inflammatory challenge disrupts the cervical epithelial barrier and promotes cervical remodeling.

STUDY DESIGN:

Immortalized ectocervical and endocervical cells were treated with lipopolysaccharide (LPS), and interleukin (IL)-6, IL-8, and soluble E-cadherin (SECAD) were assessed. Cells were then pretreated with dexamethasone prior to LPS exposure, and IL-6, IL-8, and SECAD levels were again assessed. The integrity of the epithelial cell barrier was determined using a permeability assay.

RESULTS:

LPS significantly increased IL-6 and IL-8 levels, and SECAD was significantly increased at 24 hours. LPS induced inflammation increased permeability for both cell lines. Dexamethasone pretreatment prior to LPS exposure significantly decreased IL-6 and IL-8 levels in both cell lines. There was no reduction in SECAD levels with dexamethasone pretreatment. Permeability decreased in the presence of dexamethasone for ectocervical cells only.

CONCLUSION:

These studies demonstrate an inflammatory challenge to cervical epithelial cells promotes a cytokine release and functionally alters the cervical epithelial barrier.

Copyright © 2012 Mosby, Inc. All rights reserved.

PMID:
22285171
[PubMed - indexed for MEDLINE]
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