ISSN:
1365-2222
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
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-β and IL-10, the Th2-type cytokines IL-4 and IL-6, and the Th1-type cytokines IFN-γ, TNF-α, 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-β compared with healthy skin (P 〈 0.05). Higher levels of IFN-γ, TNF-α 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-β, 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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1046/j.1365-2222.2002.01356.x
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