Hinden, Sandro; Klukowska-Rötzler, Jolanta; Janda, Jozef; Marti, Eliane Isabelle; Gerber, Vinzenz; Roosje, Petra (2012). Characterization of the inflammatory infiltrate and cytokine expression in the skin of horses with recurrent urticaria. Veterinary dermatology, 23(6), 503-e99. Blackwell Science 10.1111/j.1365-3164.2012.01117.x
Full text not available from this repository.BACKGROUND
Recurrent urticaria (RU) is a common skin disease of horses, but little is known about its pathogenesis.
HYPOTHESIS/OBJECTIVE
The aim of this study was to characterize the inflammatory cell infiltrate and cytokine expression pattern in the skin of horses with RU.
ANIMALS
Biopsies of lesional and nonlesional skin of horses with RU (n = 8) and of skin from healthy control horses (n = 8) were evaluated.
METHODS
The inflammatory cell infiltrate was analysed by routine histology. Immunohistochemistry was used to identify T cells (CD3), B ells (CD79), macrophages (MAC387) and mast cells (tryptase). Expression of T-helper 2 cytokines (interleukins IL-4, IL-5 and IL-13), a T-helper 1 cytokine (interferon-γ), IL-4 receptor α and thymic stromal lymphopoietin was assessed by quantitative RT-PCR. Results - In subepidermal lesional skin of RU-affected horses, increased numbers of eosinophils (P ≤ 0.01), CD79-positive (P ≤ 0.01), MAC387-positive (P ≤ 0.01) and tryptase-positive cells (P ≤ 0.05) were found compared with healthy horses. Subepidermal lesional skin of RU-affected horses contained more eosinophils (P ≤ 0.05) and tryptase-positive cells (P ≤ 0.05) compared with nonlesional skin. There was no significant difference in infiltrating cells between nonlesional skin and skin of healthy horses. Expression of IL-4 (P ≤ 0.01), IL-13 (P ≤ 0.05), thymic stromal lymphopoietin (P ≤ 0.05) and IL-4 receptor α (P ≤ 0.05) was increased in lesional skin of RU-affected horses compared with control horses. Expression of IL-4 was higher (P ≤ 0.05) in lesional compared with nonlesional RU skin.
CONCLUSIONS AND CLINICAL IMPORTANCE
Analysis of cytokine expression and inflammatory infiltrate suggests that T-helper 2 cytokines, eosinophils, mast cells and presumptive macrophages play a role in the pathogenesis of equine RU.