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United States Department of Agriculture

Agricultural Research Service

Title: Copper Deficiency Increases Lung and Heart Icam-1 Expression During Endotoxemia

Authors
item Schuschke, Dale - UNIV LOUISVILLE
item Percival, Susan - UNIV FLORIDA
item Lominadze, David - UNIV LOUISVILLE
item Saari, Jack
item Lentsch, Alex - UNIV LOUISVILLE

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: December 1, 2001
Publication Date: March 20, 2002
Citation: Schuschke, D., Percival, S., Lominadze, D., Saari, J.T., Lentsch, A. 2002. Copper deficiency increases lung and heart ICAM-1 expression during endotoxemia [abstract]. The Federation of American Societies for Experimental Biology Journal. 16:A990.

Technical Abstract: We have previously shown that copper deficiency increases neutrophil accumulation (as evidenced by myeloperoxidase activity) in lungs of rats. Therefore, this study evaluated if endothelial expression of the intercellular adhesion molecule-1 (ICAM-1) is copper-dependent. Male weanling rats were fed a Cu-adequate (6.0 mg Cu/kg diet) or Cu-deficient diet (0.30 mg/kg diet) for 4 weeks. ICAM-1 expression was calculated using 125**I-anti-ICAM-1 MAb within the vasculature. Inflammation was induced by endotoxin from Salmonella abortus equi (LPS). Lung, liver, heart, kidney, and skeletal muscle were measured for 125**I Mab. There was no difference in ICAM-1 expression between unstimulated dietary groups. In LPS-stimulated rats, ICAM-1 expression was greater in the lungs and hearts of the Cu- deficient group compared to the Cu-adequate group. Similar results were seen in cultured microvascular endothelial cells that had been Cu-chelated. .These results demonstrate a tissue-specific increase in LPS-induced ICAM-1 expression during copper deficiency. The findings suggest a mechanism for the exacerbated inflammatory response seen in the lungs of copper-deficient rats. Supported by NIH DK55030-02.

Last Modified: 11/28/2014
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