Premium
Evaluation of Th 1 ‐like, Th 2 ‐like and immunomodulatory cytokine mRNA expression in the skin of dogs with immunomodulatory‐responsive lymphocytic–plasmacytic pododermatitis
Author(s) -
Breathnach Rory M.,
Fanning Shay,
Mulcahy Grace,
Bassett Hugh F.,
Jones Boyd R.,
Daly Paul
Publication year - 2006
Publication title -
veterinary dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.744
H-Index - 60
eISSN - 1365-3164
pISSN - 0959-4493
DOI - 10.1111/j.1365-3164.2006.00534.x
Subject(s) - taqman , messenger rna , cytokine , real time polymerase chain reaction , transforming growth factor , interleukin , medicine , biology , immunology , microbiology and biotechnology , gene , biochemistry
The term immunomodulatory‐responsive lymphocytic–plasmacytic pododermatitis (ImR‐LPP) has previously been proposed to denote a subpopulation of dogs with idiopathic pododermatitis. The objective of this study was to quantify the expression of mRNA encoding Th 1 ‐like [interferon (IFN)‐γ, interleukin (IL)‐2 and IL‐12], Th 2 ‐like [IL‐4 and IL‐6] and immunomodulatory cytokines [IL‐10 and transforming growth factor (TGF)‐β] in lesional ImR‐LPP, nonlesional ImR‐LPP and healthy control pedal skin. Gene transcripts were quantified using TaqMan real‐time reverse transcriptase‐polymerase chain reaction assays. The skin of dogs with ImR‐LPP had significant overexpression of IL‐6 mRNA ( P < 0.05) and significant underexpression of IL‐12 mRNA ( P < 0.01) compared to healthy controls. In addition, lesional ImR‐LPP skin had significantly higher levels of IL‐10 transcripts compared to healthy control pedal skin ( P < 0.05). Although not attaining significance ( P = 0.07), a trend towards reduced TGF‐β mRNA expression in lesional ImR‐LPP skin was also evident. There were no significant differences in the levels of IFN‐γ or IL‐2 mRNA transcripts among the three skin sample sources. IL‐4 mRNA was detected in only one lesional sample. These results suggest that the pathogenesis of ImR‐LPP may be associated with a T‐cell‐mediated inflammatory response characterized by impaired Th 1 ‐like, but enhanced Th 2 ‐like cytokine expression.