J Med Microbiol International Journal of Systematic and Evolutionary Microbiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplementary Data
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yin, L.
Right arrow Articles by Dale, B. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yin, L.
Right arrow Articles by Dale, B. A.
Agricola
Right arrow Articles by Yin, L.
Right arrow Articles by Dale, B. A.
J Med Microbiol 56 (2007), 976-987; DOI: 10.1099/jmm.0.47198-0
© 2007 Society for General Microbiology
ISSN 1473-5644

Activation of protective responses in oral epithelial cells by Fusobacterium nucleatum and human ß-defensin-2

Lei Yin1 and Beverly A. Dale1,2

1 Department of Oral Biology, University of Washington, Seattle, WA, USA

2 Departments of Periodontics, Biochemistry and Medicine/Dermatology, University of Washington, Seattle, WA, USA

Correspondence
Beverly A. Dale
bdale{at}u.washington.edu

Received 31 January 2007
Accepted 13 March 2007


Oral epithelia are constantly exposed to non-pathogenic (commensal) bacteria, but generally remain healthy and uninflamed. Fusobacterium nucleatum, an oral commensal bacterium, strongly induces human ß-defensin-2 (hBD2), an antimicrobial and immunomodulatory peptide, in gingival epithelial cells (GECs). hBD2 is also expressed in normal oral tissue leading to the hypothesis that oral epithelia are in an activated state with respect to innate immune responses under normal in vivo conditions. In order to test this hypothesis, global gene expression was evaluated in GECs in response to stimulation by an F. nucleatum cell wall (FnCW) preparation and to hBD2 peptide. FnCW treatment altered 829 genes, while hBD2 altered 209 genes (P<0.005, ANOVA). Many induced genes were associated with the gene ontology categories of immune responses and defence responses. Consistent with the hypothesis, similar responses were activated by commensal bacteria and hBD2. These responses included up-regulation of common antimicrobial effectors and chemokines, and down-regulation of proliferation markers. In addition, FnCW up-regulated multiple protease inhibitors, and suppressed NF-{kappa}B function and the ubiquitin/proteasome system. These global changes may protect the tissue from inflammatory damage. Both FnCW and hBD2 also up-regulated genes that may enhance the epithelial barrier. The findings suggest that both commensal bacteria and hBD2 activate protective responses of GECs and play an important role in immune modulation in the oral cavity.


Abbreviations: EU, endotoxin unit; FnCW, Fusobacterium nucleatum cell wall; GEC, gingival epithelial cell; GO, gene ontology; hBD, human ß-defensin; IL, interleukin; PgCW, Porphyromonas gingivalis cell wall; QRT-PCR, quantitative real-time PCR; TNF, tumour necrosis factor.

A table of GEC gene expression data is available as supplementary material with the online version of this paper.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL J MED MICROBIOL MICROBIOLOGY J GEN VIROL ALL SGM JOURNALS
Copyright © 2007 Society for General Microbiology.