Effect of molybdenum-induced copper deficiency on in vivo and in vitro measures of neutrophil chemotaxis both before and following an inflammatory stressor.

Abstract

Twelve Angus x Hereford heifers (avg wt = 183.6 kg) were allotted by initial liver copper (Cu) concentrations into one of two treatments. Control (n = 6) heifers were fed a basal diet supplemented to provide a dietary Cu level of 10 ppm. Molybdenum (Mo)-induced Cu-deficient heifers (n = 6) were fed an identical basal diet supplemented with sodium molybdate (Cu:Mo ratio = 1:2.5), with dietary sulfur at .3% of the total diet. Dietary treatments were delivered for 120 d, at which time Mo-supplemented heifers were considered Cu-deficient (286 and 49 ppm liver Cu for control and Mo-induced Cu-deficient, respectively). Peripheral blood neutrophils were enumerated both before and after the administration of an inflammatory stressor, a subcutaneous injection (1.5 mL) of Freund's complete adjuvant. In vitro and in vivo measures of neutrophil chemotaxis were evaluated and the expression of two adhesion molecules, CD18 and L-selectin, were analyzed by flow cytometric procedures. Molybdenum-induced Cu deficiency increased (P < .01) the number of peripheral blood neutrophils; however, in vitro neutrophil chemotaxis was not affected. In vivo neutrophil chemotaxis tended (P < .08) to be increased in Mo-induced Cu-deficient heifers (1.55 vs 2.26 x 10(6) cells/ sponge for control and Mo-supplemented, respectively). No differences in CD18 or L-selectin expression were detected between treatments. However, CD18 expression was decreased (P < .05) in both treatments following adjuvant injection. These data suggest that Mo-induced Cu deficiency results in an increase in peripheral blood neutrophil number, without altering chemotactic ability and adhesion molecule expression.