Expression of Th1, Th2 and immunosuppressive cytokine gene transcripts in canine atopic dermatitis

Clin Exp Allergy. 2002 May;32(5):789-95. doi: 10.1046/j.1365-2222.2002.01356.x.

Abstract

Background: Atopic dermatitis is a common inflammatory skin disease of humans and dogs. Human atopic dermatitis is associated with Th2-type responses, although Th1 cytokines can be identified in chronic lesions. In contrast, tolerance to environmental allergens in healthy individuals is mediated by regulatory T cells.

Objective: This study examined the expression of the immunosuppressive cytokines TGF-beta and IL-10, the Th2-type cytokines IL-4 and IL-6, and the Th1-type cytokines IFN-gamma, TNF-alpha, IL-2, IL-12p35 and IL-12p40, in canine atopic dermatitis.

Materials and methods: RNA was isolated from lesional atopic, non-lesional atopic and healthy canine skin samples. Semi-quantitative reverse transcriptase polymerase chain reactions (RT-PCRs) were carried out using specific primers and one-way analyses of variance used to compare cytokine expression in each group.

Results: Canine atopic dermatitis was associated with over-expression of IL-4 mRNA and reduced transcription of TGF-beta compared with healthy skin (P < 0.05). Higher levels of IFN-gamma, TNF-alpha and IL-2 mRNA were seen in lesional compared with non-lesional and healthy skin (P < 0.05). There were no significant differences in IL-10, IL-6, IL-12p35 or IL-12p40 transcription between the three groups.

Conclusions: This is the first report to demonstrate that canine atopic dermatitis is associated with over-production of IL-4. Clinical tolerance in healthy individuals appears to be associated with TGF-beta, although it is unclear if this reflects an active mechanism or simply non-responsiveness of the immune system. Th1 cytokines may be induced by subsequent self-trauma and secondary infections in atopic skin. We believe that these results better characterize spontaneously occurring canine atopic dermatitis. We further propose that this should be investigated as a possible animal model of human atopic dermatitis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cytokines / genetics
  • Cytokines / immunology*
  • Dermatitis, Atopic / genetics
  • Dermatitis, Atopic / veterinary*
  • Dermatitis, Contact / genetics
  • Dermatitis, Contact / veterinary*
  • Dog Diseases / genetics*
  • Dogs
  • Humans
  • Immunosuppressive Agents / pharmacology*
  • Interleukin-10 / genetics
  • Interleukin-10 / immunology
  • RNA, Messenger / metabolism*
  • Th1 Cells / immunology*
  • Th1 Cells / metabolism*
  • Th2 Cells / immunology*
  • Th2 Cells / metabolism*
  • Transcription, Genetic
  • Transforming Growth Factor beta / immunology

Substances

  • Cytokines
  • Immunosuppressive Agents
  • RNA, Messenger
  • Transforming Growth Factor beta
  • Interleukin-10