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ORIGINAL RESEARCH ARTICLE

Impaired Deformability of Copper-Deficient Neutrophils

Sharon A. Gordon^*, David Lominadze^*, Jack T. Saari, Alex B. Lentsch and Dale A. Schuschke^*,1

^* Department of Physiology and Biophysics, University of Louisville, Louisville, Kentucky 40292; USDA, ARS, Grand Forks Human Nutrition Research Center, Grand Forks, North Dakota 58202; and Department of Surgery, University of Cincinnati, Cincinnati, Ohio 45267

To whom requests for reprints should be addressed at ¹ Department of Physiology and Biophysics, Health Sciences Center A1115, University of Louisville, Louisville, KY 40292. E-mail: daschu01{at}louisville.edu

We have previously shown that dietary copper deficiency augments neutrophil accumulation in the lung microvasculature. The current study was designed to determine whether a diet deficient in copper promotes neutrophil chemoattraction within the lung vasculature or if it alters the mechanical properties of the neutrophil, thus restricting passage through the microvessels. Sprague-Dawley rats were fed purified diets that were either copper adequate (6.3 µg Cu/g diet) or copper deficient (0.3 µg Cu/g diet) for 4 weeks. To assess neutrophil chemoattraction, bronchoalveolar lavage fluid was assayed for the neutrophil chemokine macrophage inflammatory protein-2 (MIP-2) by enzyme-linked immunosorbent assay. Neutrophil deformability was determined by measuring the pressure required to pass isolated neutrophils through a 5-µm polycarbonate filter. The MIP-2 concentration was not significantly different between the dietary groups (Cu adequate, 435.4 ± 11.9 pg/ml; Cu deficient, 425.6 ± 14.8 pg/ml). However, compared with controls, more pressure was needed to push Cu-deficient neutrophils through the filter (Cu adequate, 0.150 ± 0.032 mm Hg/sec; Cu deficient, 0.284 ± 0.037 mm Hg/sec). Staining of the filamentous actin (F-actin) with FITC-Phalloidin showed greater F-actin polymerization and shape change in the Cu-deficient group. These results suggest that dietary copper deficiency reduces the deformability of neutrophils by promoting F-actin polymerization. Because most neutrophils must deform during passage from arterioles to venules in the lungs, we propose that copper-deficient neutrophils accumulate in the lung because they are less deformable.

Key Words: inflammation • MIP-2 • F-actin