Effects of tobacco on cytokine expression from human endothelial cells

• Published in: Oral diseases 2013-10, Vol.19 (7), p.660-665
• Main Authors: Allam, E, DelaCruz, K, Ghoneima, A, Sun, J, Windsor, LJ
• Format: Article
• Language: English
• Subjects: Cardiovascular disease; Cardiovascular diseases; Cell Culture Techniques; Cell Line; Cell Proliferation - drug effects; Chemokine CCL2 - drug effects; Chemokine CXCL1 - drug effects; Cytokines; Cytokines - drug effects; Down-Regulation; endothelial cells; Endothelial Cells - drug effects; Endothelial Cells - immunology; Granulocyte-Macrophage Colony-Stimulating Factor - drug effects; Gum disease; Humans; Interleukin-10 - analysis; Interleukin-6 - analysis; Nicotine; Nicotine - pharmacology; Nicotine - toxicity; Smoke - analysis; Tobacco; Tobacco Products
• ISSN: 1354-523X; 1601-0825; 1601-0825
• DOI: 10.1111/odi.12050

Objective To investigate the effects of nicotine and cigarette smoke condensate (CSC) exposure on cytokine expression from human endothelial cells in order to identify one possible mechanism that smoking plays in the pathogenesis of both periodontal disease (PDD) and cardiovascular disease (CVD). Methods Human endothelial cells (HUVECs) were exposed to different concentrations of nicotine and CSC to examine the effects that they have on cell proliferation and cytotoxicity. Non‐toxic levels were then used to examine cytokine expression using cytokine protein arrays. Results Exposure to nicotine caused significant down‐regulation in the expression of IL‐10 (P = 0.046), growth‐regulated oncogene (GRO)α (P = 0.036), MCP‐1 (P = 0.046), and GMCSF (P = 0.004) compared with the control untreated HUVECs. Exposure to CSC caused significant down‐regulation in the expression of GRO (P = 0.04), GROα (P = 0.01), IL‐6 (P = 0.03), and MCP‐1 (P = 0.04) compared with the control untreated HUVECs. Conclusions Exposure of HUVECs to nicotine or CSC affects the levels of cytokine expression including reduction in anti‐inflammatory and chemoattractant cytokines. This may subsequently affect the host defensive mechanisms of the tissues. The action of toxic chemicals in tobacco smoke on endothelial cells is a potential pathogenic mechanism that may in part explain the association between tobacco, PDD, and CVD.