Levels of Tumor Necrosis Factor-α (TNF-α) and Soluble TNF Receptors in Chronic Venous Leg Ulcers – Correlations to Healing Status

This study tested the hypothesis that excessive tumor necrosis factor-α (TNF-α) levels in chronic venous leg ulcers are associated with impaired healing. TNF-α was measured by two enzyme-linked immunosorbent assays and a bioassay (KYM-1D4) in paired wound fluid samples collected during the nonhealin...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of investigative dermatology 1998-03, Vol.110 (3), p.292-296
Hauptverfasser: Wallace, Hilary J., Stacey, Michael C.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:This study tested the hypothesis that excessive tumor necrosis factor-α (TNF-α) levels in chronic venous leg ulcers are associated with impaired healing. TNF-α was measured by two enzyme-linked immunosorbent assays and a bioassay (KYM-1D4) in paired wound fluid samples collected during the nonhealing and healing phases from 21 human patients with venous leg ulcers. Soluble TNF receptor levels (p55 and p75) were also measured. The levels of immunoreactive TNF-α were significantly higher in wound fluid from nonhealing ulcers than in wound fluid from healing ulcers (p < 0.005), whereas the levels of bioactive TNF-α were not. Statistical analysis confirmed that TNF-α bioactivity relative to the amount of immunoreactive TNF-α was downregulated in wound fluid from nonhealing ulcers compared with healing ulcers. The levels of soluble p55 and p75 receptors in wound fluid showed a significant linear correlation (p < 0.001), suggesting a partially coordinated or common regulatory mechanism for the cleavage of transmembrane TNF receptors in chronic venous ulcers in vivo. Although the levels of soluble p75 receptors were significantly higher in nonhealing wound fluid compared with healing wound fluid (p < 0.025), these levels were theoretically inadequate to substantially neutralize the bioactivity of the accompanying TNF-α levels on their own. The bioactivity accompanying the elevated levels of immunoreactive TNF-α in wound fluid from nonhealing ulcers may have been further down-modulated by an additional mechanism. Because healing was initiated without a significant decline in the level of bioactive TNF-α, TNF-α-mediated events may not be the key events contributing to the impaired healing seen in chronic venous ulcers.
ISSN:0022-202X
1523-1747
DOI:10.1046/j.1523-1747.1998.00113.x