Medical Article Doc, Why Does My Dog Scratch? (cont.)


Cytokine Dysregulation and Janus Kinase Cytokines are signaling proteins that are released by one cell in order to communicate with another cell. A class of cytokines called interleukins (IL) can have proinflammatory or anti-inflammatory effects. Additionally, excessive IL-31 can stimulate severe pruritus and alopecia.8


of T-helper type 2 cytokines (such as IL-4, IL-5, IL-13, and IL-31) has been seen in the skin of dogs with AD. These cytokines are proinflammatory and help trigger the clinical signs associated with AD.


The Janus kinase (JAK) enzymes contribute to the activity of many cytokines. The JAK enzymes activate after proinflammatory and allergic cytokines bind to their corresponding receptors. Activated JAK enzymes then allow other signaling proteins to communicate with the cell’s nucleus, thereby generating a cellular response. Many of the dysregulated cytokines involved in AD rely on JAK activation in order to stimulate inflammation and pruritus. The inhibition of the cytokines can improve the clinical signs of dogs with AD.9


Conclusion


Atopic dermatitis is a multifactorial disease that originates in a variety of ways: allergen-specific IgE reactions, skin barrier defects, and cytokine dysregulation. There is even evidence that indicates that bacterial and yeast infections that are often thought to occur as a result of atopic skin changes may in fact contribute to its pathogenesis.10


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complexity is that the pathogenesis may vary between individuals.


Overproduction


It is unlikely that Mrs. Smith wants to hear about ceramides or cytokines when she asks why her dog is still scratching. What she wants is a treatment plan that will improve Max’s pruritus. As Max’s veterinarian, you need to consider all possible causes of his AD in order to choose a multimodal therapy best suited to his needs.


References 1. Favrot C, Steffan J, Seewald W, Picco F. A prospective study on the clinical features of chronic canine atopic dermatitis and its diagnosis. Vet Dermatol. 2010;21(1):23-31.


2. Koch SN. What is new in the diagnosis and management of canine atopic dermatitis? Today’s Veterinary Practice. 2015;May/June:95-102.


3. Marsella R. An update on the treatment of canine atopic dermatitis. Veterinary Medicine: Research and Reports. 2012;3:85-91.


4. DeBoer DJ. Canine atopic dermatitis: new targets, new therapies. J Nutr. 2004/134(8 Suppl):2056S-2061S.


5. Downing DT. Lipid and protein structures in the permeability barrier of mammalian epidermis. J Lipid Res. 1992;33:301-313.


6. Olivry T. Is the skin barrier abnormal in dogs with atopic dermatitis? Vet Immunol Immunopathol. 2011;144:11-16.


7. Olivry T, Dunston SM. Expression patterns of superficial epidermal adhesion molecules in an experimental dog model of acute atopic dermatitis skin lesions. Vet Dermatol. 2015;26:53-56.


8. Gonzales AJ, Humphrey WR, Messamore JE, Fleck TJ, Fici GJ, Shelly JA, et al. Interleukin-31: its role in canine pruritus and naturally occurring canine atopic dermatitis. Vet Dermatol. 2013;24:48-e12.


9. Gonzales AJ, Bowman JW, Fici GJ, Zhang M, Mann DW, Mitton-Fry M. Oclacitinib (APOQUEL®


) is a novel Janus kinase inhibitor with activity against cytokines involved in allergy. J Vet Pharmacol Ther. 2014;37(4):317-324.


10. DeBoer DJ, Marsella. The ACVD task force on canine atopic dermatitis (XII): the relationship of cutaneous infections to the pathogenesis and clinical course of canine atopic dermatitis. Vet Immunol Immunopathol. 2001;81:239-249.


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