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

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...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Tiszlavicz Zoltán László
Endrész Valéria
Németh Balázs Csaba
Megyeri Klára
Orosz László
Seprényi György
Mándi Yvette
Dokumentumtípus: Cikk
Megjelent: SAGE Publications 2011
Sorozat:INNATE IMMUNITY 17 No. 5
doi:10.1177/1753425910375582

mtmt:1739152
Online Access:http://publicatio.bibl.u-szeged.hu/13498
Leíró adatok
Tartalmi kivonat: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 24h. 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 24h 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. © 2011 The Author(s).
Terjedelem/Fizikai jellemzők:463-469
ISSN:1753-4259