| First Author | Na K | Year | 2007 |
| Journal | J Invest Dermatol | Volume | 127 |
| Issue | 8 | Pages | 1930-7 |
| PubMed ID | 17392825 | Mgi Jnum | J:141732 |
| Mgi Id | MGI:3819324 | Doi | 10.1038/sj.jid.5700802 |
| Citation | Na K, et al. (2007) EC-SOD suppresses contact hypersensitivity in mouse skin by impairing Langerhans cell migration. J Invest Dermatol 127(8):1930-7 |
| abstractText | 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. |
