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Staphylococcal lipoteichoic acid inhibits delayed-type hypersensitivity reactions via the platelet-activating factor receptor.

Zhang Q, Mousdicas N, Yi Q, Al-Hassani M, Billings SD, Perkins SM, Howard KM, Ishii S, Shimizu T, Travers JB

Department of Dermatology, Department of Pediatrics and the H.B. Wells Center for Pediatric Research, Department of Pathology and Laboratory Medicine, and Division of Biostatistics, Indiana University School of Medicine, Indianapolis, Indiana, USA. Department of Biochemistry, University of Texas Health Sciences Center, San Antonio, Texas, USA. Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Tokyo, Tokyo, Japan. Department of Pharmacology and Toxicology and Richard L. Roudebush V.A. Medical Center, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Staphylococcus aureus infections are known triggers for skin inflammation and can modulate immune responses. The present studies used model systems consisting of platelet-activating factor receptor-positive and -negative (PAF-R-positive and -negative) cells and PAF-R-deficient mice to demonstrate that staphylococcal lipoteichoic acid (LTA), a constituent of Gram-positive bacteria cell walls, acts as a PAF-R agonist. We show that LTA stimulates an immediate intracellular Ca flux only in PAF-R-positive cells. Intradermal injections of LTA and the PAF-R agonist 1-hexadecyl-2-N-methylcarbamoyl glycerophosphocholine (CPAF) induced cutaneous inflammation in wild-type but not PAF-R-deficient mice. Systemic exposure to LTA or CPAF inhibited delayed-type hypersensitivity (DTH) reactions to the chemical dinitrofluorobenzene only in PAF-R-expressing mice. The inhibition of DTH reactions was abrogated by the addition of neutralizing antibodies to IL-10. Finally, we measured levels of LTA that were adequate to stimulate PAF-R in vitro on the skin of subjects with infected atopic dermatitis. Based on these studies, we propose that LTA exerts immunomodulatory effects via the PAF-R through production of the Th2 cytokine IL-10. These findings show a novel mechanism by which staphylococcal infections can inhibit Th1 reactions and thus worsen Th2 skin diseases, such as atopic dermatitis.

Published 3 October 2005 in J Clin Invest, 115(10): 2855-2861.
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