Tumor necrosis factor-alpha inhibits in vivo collagen synthesis

In this study we sought to determine the in vivo role of tumor necrosis factor-alpha (TNF-alpha) at the wound-healing site. In vivo abrogation of endogenous TNF-alpha activity in experimental wounds by administration of anti-murine TNF-alpha rabbit serum resulted in a significant 77.5% increase in w...

Full description

Saved in:
Bibliographic Details
Published inSurgery Vol. 113; no. 2; p. 173
Main Authors Regan, M C, Kirk, S J, Hurson, M, Sodeyama, M, Wasserkrug, H L, Barbul, A
Format Journal Article
LanguageEnglish
Published United States 01.02.1993
Subjects
Animals
Antibodies - pharmacology
Collagen - biosynthesis
Down-Regulation - physiology
Hydroxyproline - drug effects
Hydroxyproline - physiology
Indomethacin - pharmacology
Male
Mice
Mice, Inbred BALB C
Recombinant Proteins
Tumor Necrosis Factor-alpha - immunology
Tumor Necrosis Factor-alpha - pharmacology
Tumor Necrosis Factor-alpha - physiology
Wound Healing - physiology
Online AccessGet more information

Cover

More Information
Summary:In this study we sought to determine the in vivo role of tumor necrosis factor-alpha (TNF-alpha) at the wound-healing site. In vivo abrogation of endogenous TNF-alpha activity in experimental wounds by administration of anti-murine TNF-alpha 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-alpha into subcutaneously inserted polyvinyl alcohol sponges resulted in an increase in collagen deposition (1594 +/- 117 vs 1014 +/- 49 and 1588 +/- 135 vs 1014 +/- 49 micrograms/100 mg sponge, for TNF-alpha in situ administration at a dose of 0.05 and 0.5 micrograms, 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-alpha administration is a consequence of a nonspecific inflammatory activity that indirectly promotes collagen synthesis. The data also support the hypothesis that endogenous wound TNF-alpha down-regulates collagen synthesis during normal wound healing.
ISSN:0039-6060