Expression of human {beta}-defensin-2 gene induced by CpG-DNA in human B cells

Defensins have a broad range of antimicrobial activity against bacteria, fungi, and viruses. The expression of human {beta}-defensin-2 (hBD-2) is prevalently observed in epithelial cells and is induced by bacterial infection. Here, we have shown that the expression of the hBD-2 gene and release of h...

Full description

Saved in:
Bibliographic Details
Published in:Biochemical and biophysical research communications 2009-11, Vol.389 (3)
Main Authors: Han, Su Ho, Kim, Young-Eun, Park, Jeong-A, Park, Jae-Bong, Kim, Yong-Sun, Lee, Younghee, Choi, Ihn-Geun, Kwon, Hyung-Joo, Center for Medical Science Research, College of Medicine, Hallym University, Gangwon-do 200-702
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
BACTERIA
DNA
FUNGI
GENES
INFECTIOUS DISEASES
INHIBITION
LYMPHOCYTES
PROTEINS
VIRUSES
VISIBLE RADIATION
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Defensins have a broad range of antimicrobial activity against bacteria, fungi, and viruses. The expression of human {beta}-defensin-2 (hBD-2) is prevalently observed in epithelial cells and is induced by bacterial infection. Here, we have shown that the expression of the hBD-2 gene and release of hBD-2 protein into the medium is up-regulated in response to CpG-DNA in human B cell line RPMI 8226. The induction of hBD-2 was dependent on CG sequence and phosphorothioate backbone-modification. This was also confirmed in primary human lymphocytes. To shed light on the molecular mechanism involved in hBD-2 induction by CpG-DNA, we examined the contribution of the NF-{kappa}B signaling pathway in RPMI 8226 cells. Suppression of MyD88 function and inhibition of NF-{kappa}B nuclear localization blocked hBD-2 induction. The NF-{kappa}B pathway inhibitors also abolished hBD-2 induction. These results may contribute to a better understanding on the therapeutic effects of CpG-DNA against infectious diseases.
ISSN:0006-291X
1090-2104
DOI:10.1016/J.BBRC.2009.08.162