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]
