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

Authors

  • Angela MacIntyre,

    1. Department of Biomedical Sciences, Philadelphia College of Osteopathic Medicine, 4170 City Ave., Philadelphia, PA 19131, USA
    Search for more papers by this author
  • Christine J Hammond,

    1. Department of Pathology/Microbiology and Immunology, Philadelphia College of Osteopathic Medicine, 4170 City Ave., Philadelphia, PA 19131, USA
    Search for more papers by this author
  • C.Scott Little,

    1. Department of Pathology/Microbiology and Immunology, Philadelphia College of Osteopathic Medicine, 4170 City Ave., Philadelphia, PA 19131, USA
    Search for more papers by this author
  • Denah M Appelt,

    1. Department of Biomedical Sciences, Philadelphia College of Osteopathic Medicine, 4170 City Ave., Philadelphia, PA 19131, USA
    Search for more papers by this author
  • Brian J Balin

    Corresponding author
    1. Department of Pathology/Microbiology and Immunology, Philadelphia College of Osteopathic Medicine, 4170 City Ave., Philadelphia, PA 19131, USA
      *Corresponding author. Tel.: +1 (215) 871-6862; Fax: +1 (215) 871-6869, E-mail address: brianba@pcom.edu
    Search for more papers by this author

*Corresponding author. Tel.: +1 (215) 871-6862; Fax: +1 (215) 871-6869, E-mail address: brianba@pcom.edu

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 β-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.

Ancillary