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Interleukin-6 treatment augments cutaneous wound healing in immunosuppressed mice.
Gallucci RM; Sugawara T; Yucesoy B; Berry Ann K; Simeonova PP; Matheson JM; Luster MI
J Interferon Cytokine Res 2001 Aug; 21(8):603-609
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.
Animal-studies; Laboratory-animals; Statistical-analysis; Ethanols; Biopsy; Animals; Injuries
Issue of Publication
Journal of Interferon & Cytokine Research
Page last reviewed: September 2, 2020
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