2234: Basophil/Mast Cell Response to Lectins as a Predictor for Risk of Allergic Disease in Genetically Susceptible Dogs

Grant Status: Closed

Grant Amount: $89,069.54
Bruce Hammerberg, DVM, PhD; North Carolina State University
March 8, 2002 - March 31, 2005

Sponsor(s): American Belgian Tervuren Club, Inc., American Miniature Schnauzer Club, Inc., American Sealyham Terrier Club, Bearded Collie Club of America, Bedlington Terrier Club of America, Bichon Frise Club of America, Inc., Bull Terrier Welfare Foundation, Chow Chow Club, Inc., Dalmatian Club of America Foundation, Inc., French Bulldog Club of America, Irish Water Spaniel Club of America, Otterhound Club of America, Rhodesian Ridgeback Club of the United States, Scottish Terrier Club of America, Welsh Terrier Club of America, Inc., Westie Foundation of America, Inc.

Breed(s): -All Dogs
Research Program Area: Dermatology and Allergic Disease
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Atopic dermatitis or skin allergies is a chronic debilitating disease that is widely distributed among the breeds of dogs. This inherited disease is listed as a high research priority for the following breeds: Bichon Frise, Boston Terrier, Bull Terrier, Cairn Terrier , Dalmatian, Vizsla, Welsh Terrier and West Highland White Terrier. The skin mast cell and circulating basophil are the cells mainly responsible for itching and skin damage seen in atopic dermatitis. This laboratory has just recently discovered that mast cells from atopic dogs release significantly more of the inflammatory mediator, tumor necrosis factor alpha (TNF-?), than normal dog mast cells when stimulated with lectins that bind glycoproteins on the surface of mast cells. If there is an inherited difference in how surface glycoproteins signal release of TNF-?, then knowledge of the molecular basis for this difference will lead to being able to identify dogs that will have a higher risk of developing atopic dermatitis. To accomplish this, atopic and nonatopic dogs will be compared with regard to the identity and quantity of the cell surface glycoproteins on basophils that are responsible for signaling immediate TNF-? release stimulated by lectins.


None at this time.

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