The Effect of Nicotine on Human Lymphocyte IL-6 Production

Abstract

Studies have suggested that the immune system may play important roles in the regulation of bone remodeling through cytokines secreted by inflammatory cells migrating from periodontal ligament capillaries after orthodontic force application. There is evidence that tobacco usage has profound effects on bone metabolism. The mechanism of nicotine on bone metabolism is not fully understood. One possibility may be related to certain cytokines. Cytokines are hormone-like molecules. They are important in regulating the development of the immune system and mediating immune responses. Interleukin 6 is an important cytokine secreted by activated T cells. IL-6 is a multifunctional interleukin with significant effects on different cell types. IL-6 can regulate the development and function of osteoblasts and osteoclasts, and thus play important roles in bone remodeling during orthodontic tooth movement.

Nicotine is the major pharmacological component of tobacco. It can exert effects directly on lymphocytes by signaling through nicotinic acetylcholine receptors. Nicotine has profound effects on cytokine production in the immune system. The effect of nicotine on T cell IL-6 production may have an important impact on bone remodeling. However, the effects of nicotine on human T cell IL-6 production have not been extensively studied.

The purpose of this study was to determine whether nicotine affects T cell proliferation and IL-6 production by activated T cells. Also the effect of nicotine on T cell activation was studied. The H9 cell line derived from a human cutaneous T cell lymphoma was used as the human T cells in this study. 2x106/ml T cells cultured with different mitogens were stimulated with nicotine for 24, 48, and 72 hr. The chosen nicotine concentrations were 0; 1; 10; 100; 1,000; 3,000; and 10,000 ug/ml. The effects of nicotine on T cell proliferation, T cell metabolic activity, and IL-6 production were studied. Also, the effects of different mitogens on T cell activation were studied. The results demonstrated that high concentrations of nicotine (1,000; 3,000; and 10,000 ug/ml) significantly decreased T cell proliferation, T cell metabolic activity, and IL-6 production. A medium concentration of nicotine (100 ug/ml) slightly increased IL-6 production. This study also demonstrated that TP A is essential in induction of IL-6 from activated T cells. PHA has synergistic effects on TPA induced IL-6 production. ConA, PHA, PHA+ IL β and nicotine did not induce IL-6 production from T cells. Signal transduction is probably involved in this complex process. The results of this study suggested that nicotine has adverse effects on T cell functions.