Tissue-specific ICAM-1 expression and neutrophil transmigration in the copper-deficient rat.
Dietary copper deficiency promotes neutrophil accumulation in rat lungs. We have now investigated the potential mechanisms of this effect. Male weanling rats were fed a Cu-adequate (6.0 mg diet) or Cu-deficient diet (0.30 mg) for 4 wks. Endothelial intercellular adhesion molecule-1 (ICAM-1) expression was measured in vivo and in vitro using a radiolabeled monoclonal antibody to rat ICAM-1. Tissue neutrophil accumulation was measured by myeloperoxidase (MPO) content and neutrophil transendothelial migration was assessed in vitro. Dietary copper deficiency had no effects on the expression of ICAM-1 in lung, liver, heart, kidney, or cremaster. However, MPO content was significantly greater in the lungs of copper-deficient rats. Endotoxin-induced ICAM-1 expression was greater in the lungs and hearts of copper-deficient rats. Similarly, cultured rat endothelial cells that were Cu-chelated expressed more ICAM-1 after endotoxin. This correlated with the significant increase in MPO in lungs of copper-deficient rats treated with endotoxin. The results suggest a tissue-specific difference in ICAM-1 expression and neutrophil accumulation during inflammation in copper-deficient rats. The findings suggest that lung inflammatory mechanisms are particularly sensitive to copper deficiency.
Schuschke
Dale A
DA
Department of Physiology and Biophysics, University of Louisville, Louisville, KY 40292, USA. daschu01@louisville.edu
Percival
Susan S
SS
Lominadze
David
D
Saari
Jack T
JT
Lentsch
Alex B
AB
D000818:Animals; D002465:Cell Movement / Q000502:physiology; D003300:Copper / Q000172:deficiency*; D005786:Gene Expression Regulation / Q000502:physiology; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis*; D008297:Male; D009504:Neutrophils / Q000166:cytology* / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
D018799:Intercellular Adhesion Molecule-1; D003300:Copper