Interleukin-6 treatment augments cutaneous wound healing in immunosuppressed mice

It has been postulated that the inflammatory response that occurs after cut aneous wounding is a prerequisite for healing and that inflammatory cytokin es, such as interleukin-6 (IL-6) are involved in this process. We showed pr eviously that IL-6-deficient mice display delayed wound healing, which coul d be reversed by administration of a murine IL-6 expression plasmid or reco mbinant murine IL-6 (rMuIL-6). In the present study, we observed that delay ed cutaneous wound healing, which occurs as a result of glucocorticoid-indu ced immunosuppression, can also be reversed by rMuIL-6, as evidenced by epi thelialization, granulation tissue formation, and wound closure. In vehicle control mice, rMuIL-6 did not augment healing but rather delayed the proce ss. Immunochemical studies indicated that the expression of matrix metallop roteinase-10 (MMP-10) was increased in dexamethasone-treated mice and that rMuIL-6 treatment reduced its expression, indicating that IL-6 may influenc e dermal matrix formation and, specifically, collagen synthesis. These resu lts demonstrate that IL-6 can restore abnormal wound repair that occurs in immunodeficiency and suggest its use as a potential therapy.