Effect of homocysteine on cytokine production by human endothelial cells and monocytes

Ann Clin Biochem 2003;40:534-541
doi:10.1258/000456303322326452
© 2003 Association for Clinical Biochemistry

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Original Articles


S Dalal,
SM Parkin,
S Homer-Vanniasinkam and
A Nicolaou


Department of Biomedical Sciences, University of Bradford, Richmond Road, Bradford BD7 1DP, UK;
Department of Biomedical Sciences, University of Bradford, Richmond Road, Bradford BD7 1DP, UK;
Vascular Surgical Unit, The General Infirmary at Leeds, Leeds, UK;
School of Pharmacy, University of Bradford, Richmond Road, Bradford BD7 1DP, UK


Background: Hyperhomocysteinaemia is an independent risk factorin the development of cardiovascular disease. Although homocysteinehas been shown to affect endothelial cell function, the mechanismsby which it induces disease states are still poorly understood.Here, we report the ability of homocysteine to influence inflammatorycytokine/chemokine production by human saphenous vein endothelialcells, peripheral blood monocytes and monocyte-derived macrophages.

Methods: Human saphenous vein endothelial cells, peripheral blood monocytes and monocyte-derived macrophages were treated with homocysteine (0.1-5 mmol/L) for 4 and/or 24h. Tumour necrosis factor (TNF)-{alpha}, interleukin (IL)-1β, IL-6 and IL-8 productionwas measured in the cell culture media using commercially availableenzyme-linked immunosorbent assays.

Results: Interleukin-6 production by human saphenous vein endothelial cells was significantly stimulated following a 24-h treatment with homocysteine, whilst IL-8 concentrations were inhibited after both 4- and 24-h treatments. Homocysteine was also found to stimulate IL-1β production by human peripheral blood monocytes and TNF-{alpha} production by monocyte-derived macrophages.

Conclusions: Overall, results from this study suggest that homocysteinealters the profile of cytokine/chemokine production by endothelialcells and macrophages. This altered profile may be importantin the inflammatory events that initiate or enhance the developmentof atherosclerotic lesions.


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