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Clinical and Diagnostic Laboratory Immunology, January 2003, p. 161-166, Vol. 10, No. 1
1071-412X/03/$08.00+0     DOI: 10.1128/CDLI.10.1.161-166.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Keratinocyte Expression of Human ß Defensin 2 following Bacterial Infection: Role in Cutaneous Host Defense

James G. H. Dinulos,^1, Laurel Mentele,² L. Page Fredericks,³ Beverly A. Dale,^1,3,4 and Gary L. Darmstadt^5,6*

Division of Dermatology, Department of Medicine,¹ Department of Oral Biology,³ Department of Biochemistry, University of Washington,⁴ Division of Infectious Diseases, Department of Pediatrics, University of Washington School of Medicine and Children's Hospital and Regional Medical Center, Seattle, Washington,² Office of Health, Save the Children Federation, Washington, D.C.,⁵ Division of Community Health and Health Systems, Department of International Health, Bloomberg School of Public Health, The Johns Hopkins Medical Institutions, Baltimore, Maryland⁶

Received 17 April 2002/ Returned for modification 11 August 2002/ Accepted 8 October 2002

Human ß defensin 2 (hßD-2) is thought to play an important role in cutaneous immune defense. We hypothesized that (i) keratinocyte expression of hßD-2, measured by reverse transcription-PCR, would be upregulated in response to challenge with pathogenic bacteria, particularly highly adherent strains of Streptococcus pyogenes and Staphylococcus aureus, and (ii) hßD-2 would have potent antimicrobial activity against pathogenic but not commensal organisms. Expression of hßD-2 was induced consistently by S. aureus, Staphylococcus epidermidis, Escherichia coli, and Pseudomonas aeruginosa, whereas strains of S. pyogenes were poor and variable inducers of hßD-2. No correlation was found between levels of bacterial adherence and keratinocyte expression of hßD-2. S. pyogenes was significantly more sensitive to killing by hßD-2 than S. epidermidis. We conclude that the ability to induce hßD-2 expression in combination with sensitivity to its antimicrobial effects may contribute to the rarity of skin infections with the gram-negative bacterial organisms, whereas lack of stimulation of hßD-2 expression by S. pyogenes may be important in its ability to evade innate defenses and cause skin disease. Induction of expression of hßD-2 but relative tolerance to it may enable S. epidermidis to survive on the skin surface and modulate hßD-2 expression when the stratum corneum barrier is disrupted.

Present address: Section of Dermatology, Departments of Medicine and Pediatrics, Dartmouth Medical School, Lebanon, N.H.

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