Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 174, Issue 6, Pages 2129-2136Publisher
ELSEVIER SCIENCE INC
DOI: 10.2353/ajpath.2009.080765
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Funding
- National Institutes of Health [GM-042859, GM-066194, GM-079227, P20-RR17695]
- Molecular Pathology Core of the COBRE Center for Cancer Research Development
- National Center for Research Resources. Institutional Development Award Program
- Carter Family Trust
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR017695] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [K08GM079227, R01GM042859, R01GM066194, R56GM066194] Funding Source: NIH RePORTER
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In this study, we investigated the role of interleukin (IL)-1 signaling in wound heating. IL-1 receptor type I (IL-1R) knockout (KO) mice showed reduced fibrosis in both cutaneous and deep tissue wounds, which was accompanied by a reduction in inflammatory cellular infiltration in cutaneous but not in deep tissue wounds. There were no differences in either total collagenolytic activity or in the expression of selected matrix metalloproteinases; or tissue inhibitors of metalloproteinases between the wound fluids from wildtype or IL-1R KO mice. However, wound fluids from IL-1R KO mice contained lower levels of IL-6 compared with wild-type controls. In addition, the infusion of IL-6 into wounds in IL-1R KO mice did not increase fibrosis. Skin wounds in IL-1R KO animals had lower levels of collagen and improved restoration of normal skin architecture compared with skin wounds in wild-type mice. However, neither the tensile strength of incisional skin wounds nor the rate of closure of excisional wounds differed between IL-1R KO and wild-type animals. The reduced fibrotic response in wounds from IL-1R KO mice could be reproduced by the administration of an IL-1R antagonist. These findings suggest that pharmacological interference with IL-1 signaling could have therapeutic value in the prevention of hypertrophic scarring and in the treatment of fibrotic diseases. (Am J Pathol 2009, 174:2129-2136; DOI:10.2353/ajpath.2009.080765)
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