skip to main content
OSTI.GOV title logo U.S. Department of Energy
Office of Scientific and Technical Information

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

Journal Article · · Biochemical and Biophysical Research Communications
 [1]; ;  [2];  [3];  [1];  [2];  [4];  [1]
  1. Department of Microbiology, College of Medicine, Hallym University, Gangwon-do 200-702 (Korea, Republic of)
  2. Department of Biochemistry, College of Natural Sciences, Chungbuk National University, Chungbuk 361-763 (Korea, Republic of)
  3. Department of Biochemistry, College of Medicine, Hallym University, Gangwon-do 200-702 (Korea, Republic of)
  4. Department of Neuropsychiatry, Hallym University, Han-Gang Sacred Heart Hospital, Seoul 150-719 (Korea, Republic of)

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.

OSTI ID:
22199879
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 389, Issue 3; Other Information: Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English