FEMS Microbiol Lett 2002 Dec 17;217(2):167-172
MacIntyre A, Hammond CJ, Little CS, Appelt DM, Balin BJ.
Department of Biomedical Sciences, Philadelphia College of Osteopathic Medicine, 4170 City Ave., 19131, Philadelphia, PA, USA
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 beta-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.