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Infection and Immunity, January 2004, p. 352-358, Vol. 72, No. 1
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.1.352-358.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Innate Immune Response of Oral and Foreskin Keratinocytes: Utilization of Different Signaling Pathways by Various Bacterial Species

Whasun O. Chung* and Beverly A. Dale

Department of Oral Biology, University of Washington, Seattle, Washington 98195-7132

Received 4 June 2003/ Returned for modification 26 July 2003/ Accepted 26 September 2003

The innate immune response is critical for the epithelial antimicrobial barrier. The human ß-defensins are small, cationic antimicrobial peptides that are made by epithelial cells and that play a role in mucosal and skin defenses. Human ß-defensin 1 (hBD-1) is expressed constitutively in epithelial tissues, whereas hBD-2 and hBD-3 are expressed in response to bacterial stimuli or inflammation. Previous studies showed that hBD-2 was induced by Fusobacterium nucleatum cell wall extract without the involvement of the NF-{kappa}B transcription factors, which typically are associated with innate immunity and inflammation. The goal of this study was to characterize signaling pathways involved in hBD-2 induction in response to commensal and pathogenic bacteria. Cultured human oral and foreskin keratinocytes were treated separately with inhibitors of NF-{kappa}B, c-Jun N-terminal kinase (JNK), and p38 and then stimulated with oral commensal Streptococcus gordonii, oral pathogens Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, skin commensal Staphylococcus epidermidis, or skin pathogen Streptococcus pyogenes. Different bacteria induced different levels of hBD-2 and in response to the various inhibitors tested, although certain common patterns were observed for commensal- and pathogen-stimulated cells. hBD-2 induction by all bacteria tested was partially or completely blocked by inhibitors of the JNK and p38 pathways. However, in addition, hBD-2 induction by pathogenic bacteria in both oral and foreskin keratinocytes was blocked by inhibitors of NF-{kappa}B. The results indicate that commensal and pathogenic bacteria utilize different pathways in hBD-2 induction and suggest that epithelial cells from different body sites have common signaling mechanisms to distinguish between commensal and pathogenic bacteria.

* Corresponding author. Mailing address: Department of Oral Biology, School of Dentistry, Box 357132, University of Washington, Seattle, WA 98195-7132. Phone: (206) 543-1595. Fax: (206) 685-3162. E-mail: sochung{at}u.washington.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, January 2004, p. 352-358, Vol. 72, No. 1
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.1.352-358.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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