Skip Navigation



International Immunology Advance Access published online on November 6, 2007
International Immunology, doi:10.1093/intimm/dxm115
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
20/1/21    most recent
dxm115v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Krisanaprakornkit, S.
Right arrow Articles by Reutrakul, V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Krisanaprakornkit, S.
Right arrow Articles by Reutrakul, V.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Involvement of phospholipase D in regulating expression of anti-microbial peptide human ß-defensin-2

Suttichai Krisanaprakornkit1, Pareena Chotjumlong2, Prachya Kongtawelert2 and Vichai Reutrakul3

1 Department of Odontology and Oral Pathology, Faculty of Dentistry
2 Thailand Excellence Center for Tissue Engineering, Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand
3 Department of Chemistry, Faculty of Science, Mahidol University, Bangkok 10400, Thailand

Correspondence to: Correspondence to: V. Reutrakul; E-mail: scvrt{at}mahidol.ac.th

Human ß-defensin expression correlates with differentiation in oral epithelium, and calcium ion, an important regulator of epithelial differentiation, plays a critical role in regulation of human ß-defensin-2 (hBD-2) mRNA expression. Phospholipase D (PLD) also regulates epithelial differentiation. Therefore, we examined the role of PLD in hBD-2 up-regulation by cell wall extract of Fusobacterium nucleatum and phorbol 12-myristate 13-acetate (PMA), two known hBD-2 activators. We found that hBD-2 mRNA up-regulation in human gingival epithelial cells (HGECs) by these two activators was mediated by PLD activation and blocked by ethanol and 1-butanol, PLD inhibitors. PLD activity was induced by stimulation with these two activators, and phosphatidic acid (PA), a product generated from the PLD enzymatic activity, was detected in stimulated HGECs. Dioctanoyl PA commonly used for PA induced hBD-2 mRNA expression. mRNAs for PLD1{alpha} and ß splice variants as well as PLD1 protein were constitutively expressed, whereas mRNA and protein for PLD2 were expressed at much lower levels than those for PLD1. Moreover, pre-treatment with (±)-propanolol, an inhibitor of phosphatidic acid phosphohydrolases that are the downstream signaling molecules in the PLD pathway, significantly blocked hBD-2 mRNA induction by PMA in a dose-dependent manner. In conclusion, these findings indicate the involvement of PLD activation in hBD-2 up-regulation in HGECs, which correlates with the state of epithelial differentiation.

Keywords: commensal bacteria, gene regulation, gingival epithelial cells, innate immunity, signal transduction

Transmitting editor: S. H. E. Haufman

Received 2 February 2007, accepted 11 October 2007.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 JDRHome page
P. Montreekachon, P. Chotjumlong, V. Reutrakul, and S. Krisanaprakornkit
Involvement of Cytosolic Phospholipase A2{alpha} in MMP-9 Up-regulation
Journal of Dental Research, November 1, 2009; 88(11): 1031 - 1036.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.