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* Division of Dermatology, Department of Medicine, University of California, San Diego and VA Medical Center, San Diego, CA 92161;
San Gallicano Dermatological Institute (Instituto di Ricovero e Cura a Carattere Scientifico), Rome, Italy;
Department of Dermatology, Weill Medical College of Cornell University, New York, NY 10021; and
Division of Dermatology, Department of Medicine, University of California, Los Angeles, CA 92161
Cathelicidins are antimicrobial peptides of the innate immune system that establish an antimicrobial barrier at epithelial interfaces and have been proposed to have a proinflammatory function. We studied the role of cathelicidin in allergic contact dermatitis, a model requiring dendritic cells of the innate immune response and T cells of the adaptive immune response. Deletion of the murine cathelicidin gene Cnlp enhanced an allergic contact response, whereas local administration of cathelicidin before sensitization inhibited the allergic response. Cathelicidins inhibited TLR4 but not TLR2 mediated induction of dendritic cell maturation and cytokine release, and this inhibition was associated with an alteration of cell membrane function and structure. Further analysis in vivo connected these observations because inhibition of sensitization by exogenous cathelicidin was dependent on the presence of functional TLR4. These observations provide evidence that cathelicidin antimicrobial peptides mediate an anti-inflammatory response in part by their activity at the membrane.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by a Veterans Administration Merit Award, National Institutes of Health/National Institute of Allergy and Infectious Diseases Grants HHSN26620040029C, ADB Contract N01-AI-40029, AI48176, AI052453, and AR45676 (to R.L.G.), and a Skin Research Grant from the Johnson & Johnson Skin Research Center (to A.D.).
2 Address correspondence and reprint requests to Dr. Richard L. Gallo, Division of Dermatology, University of California, San Diego, 3350 La Jolla Village Drive, San Diego, CA 92161. E-mail address: Rgallo{at}ucsd.edu
3 Abbreviations used in this paper: DC, dendritic cell; BMDC, bone marrow-derived DC; NHK, normal human keratinocyte; mCRAMP, mouse cathelicidin-related antimicrobial peptide.
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