Interleukin-31: its role in canine pruritus and naturally occurring canine atopic dermatitis
Background – Interleukin‐31 (IL‐31) is a member of the gp130/interleukin‐6 cytokine family that is produced by cell types such as T helper 2 lymphocytes and cutaneous lymphocyte antigen positive skin homing T cells. When overexpressed in transgenic mice, IL‐31 induces severe pruritus, alopecia and...
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Veröffentlicht in: | Veterinary dermatology 2013-02, Vol.24 (1), p.48-e12 |
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Sprache: | eng |
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Zusammenfassung: | Background – Interleukin‐31 (IL‐31) is a member of the gp130/interleukin‐6 cytokine family that is produced by cell types such as T helper 2 lymphocytes and cutaneous lymphocyte antigen positive skin homing T cells. When overexpressed in transgenic mice, IL‐31 induces severe pruritus, alopecia and skin lesions. In humans, IL‐31 serum levels correlate with the severity of atopic dermatitis in adults and children.
Hypothesis/Objective – To determine the role of IL‐31 in canine pruritus and naturally occurring canine atopic dermatitis (AD).
Animals – Purpose‐bred beagle dogs were used for laboratory studies. Serum samples were obtained from laboratory animals, nondiseased client‐owned dogs and client‐owned dogs diagnosed with naturally occurring AD.
Methods – Purpose‐bred beagle dogs were administered canine interleukin‐31 (cIL‐31) via several routes (intravenous, subcutaneous or intradermal), and pruritic behaviour was observed/quantified via video monitoring. Quantitative immunoassay techniques were employed to measure serum levels of cIL‐31 in dogs.
Results – Injection of cIL‐31 into laboratory beagle dogs caused transient episodes of pruritic behaviour regardless of the route of administration. When evaluated over a 2 h period, dogs receiving cIL‐31 exhibited a significant increase in pruritic behaviour compared with dogs that received placebo. In addition, cIL‐31 levels were detectable in 57% of dogs with naturally occurring AD (≥13 pg/mL) but were below limits of quantification ( |
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ISSN: | 0959-4493 1365-3164 |
DOI: | 10.1111/j.1365-3164.2012.01098.x |