Inducible expression of human β-defensin 2 by Chlamydophila pneumoniae in brain capillary endothelial cells

Innate Immun. 2011 Oct;17(5):463-9. doi: 10.1177/1753425910375582. Epub 2010 Jul 20.

Abstract

Defensins are an important family of natural antimicrobial peptides. Chlamydophila pneumoniae, a common cause of acute respiratory infection, has a tendency to cause persistent inflammatory diseases such as atherosclerosis, which may lead to cardiovascular disease or stroke. As endothelial cells are related to the physiopathology of stroke, the effects of in vitro C. pneumoniae infection on the expression of human β-defensin 2 (HBD-2) in brain capillary endothelial cells (BB19) was investigated. A time-dependent increase in HBD-2 mRNA was observed by means of real-time reverse transcription PCR (RT-PCR) in BB19 cells following C. pneumoniae infection, with a maximum increase at 24 h. A gradual induction of HBD-2 protein in the C. pneumoniae-infected endothelial cells was detected by immunoblotting. Immunofluorescence revealed the staining of HBD-2 in the cytoplasm of endothelial cells following C. pneumoniae infection. The secretion of HBD-2 (confirmed by ELISA) was significantly elevated 24 h after C. pneumoniae infection. These novel results indicate that HBD-2 is expressed and produced in the human brain capillary endothelial cells upon infection with C. pneumoniae, and provide evidence that HBD-2 plays a role in the early immune responses to C. pneumoniae and probably in the immunopathogenesis of atherosclerosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Brain / blood supply
  • Cell Line
  • Chlamydophila Infections / complications
  • Chlamydophila Infections / immunology*
  • Chlamydophila pneumoniae / immunology*
  • Chlamydophila pneumoniae / pathogenicity
  • Cytoplasm / metabolism
  • Endothelial Cells / immunology
  • Endothelial Cells / metabolism*
  • Endothelial Cells / microbiology
  • Endothelial Cells / pathology
  • Fluorescent Antibody Technique
  • Gene Expression Regulation / immunology
  • Humans
  • Immunity, Innate / genetics
  • Transcriptional Activation* / immunology
  • beta-Defensins / genetics
  • beta-Defensins / immunology
  • beta-Defensins / metabolism*

Substances

  • DEFB4A protein, human
  • beta-Defensins