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Zinc and copper plasma levels in Icelandic horses with Culicoides hypersensitivity
Author(s) -
STARK G.,
SCHNEIDER B.,
GEMEINER M.
Publication year - 2001
Publication title -
equine veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.82
H-Index - 87
eISSN - 2042-3306
pISSN - 0425-1644
DOI - 10.2746/042516401776254916
Subject(s) - zinc , copper , horse , zoology , cytokine , immunology , medicine , endocrinology , immune system , chemistry , biology , paleontology , organic chemistry
Summary Zinc concentration has been shown to have a potent immunomodulatory capacity, particularly influencing T helper cell organisation and cytokine secretion. Culicoides hypersensitivity (CHS) in horses resembles the early and late phase of type I hypersensitive reactions in man, characterised by a shift from T helper cell subtype 1 to T helper cell subtype 2 cytokine profile. In this pilot study, zinc and copper levels were measured in the plasma of 48 CHS‐affected and 56 healthy Icelandic horses age 4–25 years (mean ˜ 11 years) kept on 7 farms. Affected horses were divided into 3 groups according to the severity of disease. Time of blood collection and feeding management was constant. No differences in zinc or copper plasma levels and plasma copper/zinc ratio were determined among CHS horses and controls by univariate analysis of variance. Therefore, the most significant influences on zinc and copper plasma levels were affected by the location of housing. However, Spearman correlation showed a negative coefficient between the plasma zinc concentration and the severity of CHS (r =−0.31). Due to a probability value of P = 0.002 the null hypothesis r = 0 is rejected, although only 9% of the total variation of plasma zinc is presently explained by its relationship to CHS. In contrast, the Spearman correlation coefficient between plasma copper levels and severity of CHS was not significant (r =−0.14; P = 0.16). The minor deviations in plasma zinc concentrations in association with the severity of CHS may be real or due to neurohumoral or cytokine‐mediated mechanisms, but appear too minimal to be relevant.