Effect of Corticosterone on the Incidence of Amelanosis in Smyth Delayed Amelanotic Line Chickens

Abstract

The Smyth Delayed Amelanotic (SDA) line chicken exhibits a postnatal loss of pigment in feathers and choroid presumably due to an autoimmune reaction triggered by a basic pigment cell defect. The present study was designed to determine if the incidence and severity of amelanosis would be affected by administration of corticosterone (CS) in feed. The SDA line chickens were given 0, 20, 30, 40, and 50 ppm CS from 4 to 12 weeks of age. Body weight and incidence of amelanosis were determined weekly and immune response to sheep red blood cells was determined at the end of the trials. Body weight and immune response levels were significantly lower in treated groups than in controls (P less than .001), but no significant differences were found between treated groups on measures of amelanosis or immune response. Incidence of amelanosis in controls (60%) was significantly greater than in treated groups: 20 ppm, 14.2%; 30 ppm, 17.9%; 40 ppm, 12.9%; and 50 ppm, 16.7%. Six weeks posttreatment, treated groups were no longer significantly different from controls in terms of the incidence of amelanosis. It is proposed that the reduction in amelanosis during CS treatment is attributable to suppression of antibody response to the pigment cell antigen by the CS.

The role of T cells in cutaneous autoimmune disease

“…VL affects nearly 1% of the population [157] and often coexists with other autoimmune diseases, such as IDDM and Graves' disease [158]. The treatment success of immunosuppressive treatments, such as cyclosporin A [159,160], corticosteroids [161] and bursectomy in a chicken model of disease [162], underscore the importance of the host immune response in VL pathogenesis. Autoantibodies targeting various melanocyte components, such as tyrosinase and melanocytespecific protein mpel17, have been described [163][164][165][166][167][168][169][170].…”

Autoimmunity as an aetiological factor in vitiligo

“…60 In this avian model, vitiligo begins with an inherent melanocyte defect that is followed by an autoimmune response involving both humoral and cellular reactions that eliminate abnormal pigment cells. [61][62][63][64] An increase in T cells in the feather pulp and circulating inflammatory leucocytes has been shown in Smyth chickens prior to the onset, and during the development, of vitiligo. 65,66 Autoantibodies to chicken melanocytes have also been detected in the sera of 100% of Smyth chicks but not in the sera of normally pigmented birds.…”

“…The well‐documented Smyth chickens express a genetically inherited form of vitiligo‐like depigmentaton resulting from the loss of melanocytes in feather and ocular tissues 60 . In this avian model, vitiligo begins with an inherent melanocyte defect that is followed by an autoimmune response involving both humoral and cellular reactions that eliminate abnormal pigment cells 61–64 . An increase in T cells in the feather pulp and circulating inflammatory leucocytes has been shown in Smyth chickens prior to the onset, and during the development, of vitiligo 65,66 .…”

The chick eye in vision research: An excellent model for the study of ocular disease

“…Successful treatment of Smyth Line vitiligo has been demonstrated with administration of cyclosporine (Fite et al, 1986) and corticosterone (Boyle et al, 1987), producing decreased cutaneous and ocular manifestations of autoimmune amelanosis. As reviewed by Wick et al (2006), DAM chicks have been used extensively as a model for the study the genetic basis and pathophysiology of vitiligo.…”