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TNF-alpha dependent NF-kappa B activation in cultured canine keratinocytes is partly mediated by reactive oxygen

H B Köhler1, B Huchzermeyer, M Martin

  • 1Klinik für kleine Haustiere, Tierärztliche Hochschule Hannover, Bischofsholer Damm 15, 30173 Hannover, Germany. hkoehler@stud.tiho-hannover.de

Veterinary Dermatology
|June 26, 2001
PubMed

Insights

Tumor necrosis factor-alpha (TNF-alpha) activates NF-kappa B in canine skin cells, involving reactive oxygen species (ROS). Antioxidants may help manage canine skin inflammation by modulating this pathway.

Area of Science:

  • Veterinary Dermatology
  • Immunology
  • Cell Biology

Background:

  • Tumor necrosis factor-alpha (TNF-alpha) is crucial in canine skin's inflammatory and immune responses.
  • Understanding the TNF-alpha signaling pathway is key for therapeutic interventions in canine skin diseases.

Purpose of the Study:

  • To investigate the role of NF-kappa B and reactive oxygen species (ROS) in TNF-alpha signaling in canine keratinocytes.
  • To explore the potential of antioxidants in modulating this pathway for therapeutic benefit.

Main Methods:

  • Cultured canine keratinocytes were treated with TNF-alpha.
  • NF-kappa B activation was assessed.
  • Reactive oxygen species (ROS) production was measured using cytochrome c reduction test and spectroscopy.
  • Hydrogen peroxide formation was localized using electron energy loss spectroscopy (EELS).

Main Results:

  • TNF-alpha induced NF-kappa B activation, partially inhibited by alpha-lipoic acid.
  • No extracellular superoxide production was detected.
  • Intracellular hydrogen peroxide production was confirmed in TNF-alpha stimulated keratinocytes.
  • EELS revealed hydrogen peroxide formation in mitochondria, endoplasmic reticulum, cytosol, and plasma membrane.

Conclusions:

  • Reactive oxygen species (ROS) are likely involved in the TNF-alpha signaling pathway leading to NF-kappa B activation in canine skin.
  • Adjunctive therapy with antioxidants could be beneficial for canine cutaneous inflammation by modulating NF-kappa B overactivation.

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