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EC-SOD suppresses contact hypersensitivity in mouse skin by impairing Langerhans cell migration.

Na K, Kim KE, Park ST, Kim TY

Laboratory of Dermato-Immunology, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.

Extracellular superoxide dismutase (EC-SOD) is primarily a tissue enzyme and has been implicated in the modulation of inflammatory response. The biological role of EC-SOD in skin, however, has rarely been investigated. In this study, we aim to explore the effects of EC-SOD on the inflammatory response in skin by evaluating the contact hypersensitivity response (CHS) in EC-SOD transgenic mice. Transgenic mice with skin-specific expression of EC-SOD were sensitized and challenged with 2,4,6-trinitro-1-chlorobenzene (TNCB), followed by measurement of ear swelling. EC-SOD transgenic mice showed significantly reduced CHS responses compared with wild-type mice. Histological evaluation of the challenged ears of EC-SOD transgenic mice revealed diminished infiltration of inflammatory cells with a failure to induce expression of inflammatory cytokines, such as tumor necrosis factor-alpha and IFN-gamma, on sensitization and challenge with TNCB. Furthermore, Langerhans cell migration to lymph nodes was impaired in EC-SOD transgenic mice. These results indicate that EC-SOD downregulates CHS through inhibition of the inflammatory response, suggesting a possible therapeutic regimen in inflammatory skin diseases.

Published 16 July 2007 in J Invest Dermatol, 127(8): 1930-7.
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