Effect of vanadium on human dendritic cells

Abstract

Vanadium is a heavy metal that has no known biological role in humans. However, increasing exposure through advances in medical applications – orthodontic/orthopedic metal implants, vanadium-containing drugs and environmental exposure have raised questions on the influence of vanadium on the immune system. As initiators of the adaptive immune response, dendritic cells (DC) are responsible for the differentiation of effector T-lymphocytes and the resulting immune reactivity. This study assessed the differences in immune reactivity towards various vanadium compounds and investigated the influence of vanadium (III), (IV), and (V) ions on peripheral blood monocytes (PBMC) and DC. Exposure to vanadium (III) and (IV) concentrations above 125 µM reduced the proliferation of lymphocytes. Mitochondrial DC activity was reduced in the presence of low concentrations of vanadium. Flow cytometry analysis of cell surface molecules showed slight alterations of MHC class II (antigen presenting molecule) and reduction of CD54 (adhesion molecule) with increasing vanadium concentrations. Secreted cytokines and chemokines produced by DC were measured through a cytometric bead assay, which showed no significant difference after exposure to various vanadium ions. Finally, the ability of vanadium-treated DC to interact with lymphocytes was measured through proliferation of allogenic non-adherent PBMC and showed retention of proliferative capacity. These results indicate that vanadium exerts a weak influence on the maturation and function of DC, which suggests that alterations in immune reactivity by vanadium is mediated directly on effector lymphocytes.

Keywords:

• vanadium
• dendritic cell
• immune reactivity
• human
• in vitro

Acknowledgments

The authors acknowledge the facilities, scientific and technical assistance of the Australian Microscopy & Microanalysis Research Facility at the Centre for Microscopy, Characterization & Analysis, The University of Western Australia. This project was partially supported by the AO Foundation Grant 05Z34.