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Inflammation promotes a cytokine response and disrupts the cervical epithelial barrier: a possible mechanism of premature cervical remodeling and preterm birth
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 w...
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Published in: | American journal of obstetrics and gynecology 2012-03, Vol.206 (3), p.208.e1-208.e7 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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. |
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ISSN: | 0002-9378 1097-6868 |
DOI: | 10.1016/j.ajog.2011.12.036 |