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Abstract
In this study we sought to determine the in vivo role of tumor necrosis factor-α (TNF-α)
at the wound-healing site. In vivo abrogation of endogenous TNF-α activity in experimental
wounds by administration of anti-murine TNF-α rabbit serum resulted in a significant
77.5% increase in wound collagen deposition, as assessed by wound sponge granuloma
hydroxyproline content. Administration of pharmacologic doses of recombinant murine
TNF-α into subcutaneously inserted polyvinyl alcohol sponges resulted in an increase
in collagen deposition (1594 ± 777 vs 1014 ± 49 and 1588 ± 135 vs 1014 ± 49 μg/100
mg sponge, for TNF-α in situ administration at a dose of 0.05 and 0.5 μg, respectively).
This effect could be abolished by the simultaneous systemic treatment of the animals
with the antiinflammatory drug indomethacin. The data suggest that the enhanced collagen
deposition after TNF-α administration is a consequence of a nonspecific inflammatory
activity that indirectly promotes collagen synthesis. The data also support the hypothesis
that endogenous wound TNF-α down-regulates collagen synthesis during normal wound
healing.
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Article info
Publication history
Accepted:
October 25,
1991
Footnotes
☆Supported by National Institutes of Health grant R29 GM38650.
Identification
Copyright
© 1993 Published by Elsevier Inc.
