WoundReference improves clinical decisions
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Gallucci RM, Sugawara T, Yucesoy B, Berryann K, Simeonova PP, Matheson JM, Luster MI, et al.
Journal of interferon & cytokine research : the official journal of the International Socie.... Date of publication 2001 Aug 1;volume 21(8):603-9.
1. J Interferon Cytokine Res. 2001 Aug;21(8):603-9. Interleukin-6 treatment augments cutaneous wound healing in immunosuppressed mice. Gallucci RM(1), Sugawara T, Yucesoy B, Berryann K, Simeonova PP, Matheson JM, Luster MI. Author information: (1)Toxicology and Molecular Biology Branch, Health Effects Laboratory Division, NIOSH/CDCP, 1095 Willowdale Road, Morgantown, WV 26505-2888, USA. It has been postulated that the inflammatory response that occurs after cutaneous wounding is a prerequisite for healing and that inflammatory cytokines, such as interleukin-6 (IL-6) are involved in this process. We showed previously that IL-6-deficient mice display delayed wound healing, which could be reversed by administration of a murine IL-6 expression plasmid or recombinant murine IL-6 (rMuIL-6). In the present study, we observed that delayed cutaneous wound healing, which occurs as a result of glucocorticoid-induced immunosuppression, can also be reversed by rMuIL-6, as evidenced by epithelialization, granulation tissue formation, and wound closure. In vehicle control mice, rMuIL-6 did not augment healing but rather delayed the process. Immunochemical studies indicated that the expression of matrix metalloproteinase-10 (MMP-10) was increased in dexamethasone-treated mice and that rMuIL-6 treatment reduced its expression, indicating that IL-6 may influence dermal matrix formation and, specifically, collagen synthesis. These results demonstrate that IL-6 can restore abnormal wound repair that occurs in immunodeficiency and suggest its use as a potential therapy. DOI: 10.1089/10799900152547867 PMID: 11559438 [Indexed for MEDLINE]
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