Chlamydia pneumoniae infection alters the junctional complex proteins of human brain microvascular endothelial cells

Document Type

Article

Publication Date

2002

Abstract

Chlamydia pneumoniae has been identified and associated with multiple sclerosis (MS) and Alzheimer's disease (AD) pathogenesis, although the relationship of this organism in these diseases remains controversial. We have hypothesized that one potential avenue of infection is through the junctional complexes between the blood-brain barrier (BBB) endothelia. C. pneumoniae is characteristically a respiratory pathogen, but has been implicated in atherosclerosis, coronary artery disease, and neuroinflammatory conditions. C. pneumoniae infection may lead to endothelial damage, junctional alterations, and BBB breakdown. Therefore, in this study, C. pneumoniae infection of human brain microvascular endothelial cells (HBMECs) resulted in increased expression of the zonula adherens proteins ß-catenin, N-cadherin, and VE-cadherin, and decreased expression of the tight junctional protein occludin, as determined by immunocytochemistry and Western blot analyses. These events may underlie a mechanism for the regulation of paracellular permeability while maintaining barrier integrity during C. pneumoniae infection associated with neuropathologies such as MS and AD.

Publication Title

FEMS microbiology letters

Volume

217

Issue

2

First Page

167

Last Page

172

Comments

This article was published in FEMS microbiology letters, Volume 217, Issue 2, Pages 167-172.

The published version is available at http://dx.doi.org/10.1016/S0378-1097(02)01066-2.

Copyright © 2002 FEMS.

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