title: Nicotine modulation of cytokine induction by LPS-stimulated human monocytes and coronary artery endothelial cells.
abstract: Nicotine, the major addictive component of tobacco, is an immunomodulator that impacts on many cells, including immune cells involved in inflammatory processes. Nicotine also induces oxidative damage to the vascular endothelium and accentuates lipid peroxidation, resulting in vascular cell dysfunction. Furthermore, vascular endothelial cells produce growth factors, such as cytokines and chemokines capable of stimulating and recruiting immune cells to atheromatous lesions. In addition, bacterial products including lipopolysaccharides (LPS), a major component of Gram negative bacterial cell walls, activate gene expression resulting in inflammatory cytokine production causing further damage to the vasculature. In the present study, the combined effects of nicotine and bacterial LPS on the expression of IL-6, IL-8, GRO-alpha and MCP-1 in cell lines of human coronary artery endothelial cells (HCAEC) and pulmonary monocytes (THP-1) were examined by quantitative real-time PCR and ELISA. Results showed that nicotine suppressed the LPS induced production of IL-6 and IL-8 in both cell lines. Since cytokines which alter homeostasis of both vascular endothelial and immune cells are critical for the atherogenic process, further studies are warranted to examine in detail the role of nicotine in terms of effects on inflammatory reactions, including those induced by bacterial infection.
authors.affiliation: Department of Medical Microbiology and Immunology, College of Medicine, University of South Florida, MDC-10, 12901 Bruce B. Downs Blvd., Tampa, FL 33612-4742, United States.
authors.forename: G W
authors.initials: GW
authors.lastname: Patton
authors.forename: D A
authors.initials: DA
authors.lastname: Powell
authors.forename: A
authors.initials: A
authors.lastname: Hakki
authors.forename: H
authors.initials: H
authors.lastname: Friedman
authors.forename: S
authors.initials: S
authors.lastname: Pross
mesh_terms: D050197:Atherosclerosis / Q000209:etiology; D002460:Cell Line; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000235:genetics; D054360:Chemokine CXCL1; D019743:Chemokines, CXC / Q000096:biosynthesis / Q000235:genetics; D003331:Coronary Vessels / Q000187:drug effects / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000276:immunology*; D006801:Humans; D007239:Infections / Q000150:complications; D036341:Intercellular Signaling Peptides and Proteins / Q000096:biosynthesis / Q000235:genetics; D015850:Interleukin-6 / Q000096:biosynthesis / Q000235:genetics; D016209:Interleukin-8 / Q000096:biosynthesis / Q000235:genetics; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000633:toxicity*; D009000:Monocytes / Q000187:drug effects* / Q000276:immunology*; D009538:Nicotine / Q000008:administration & dosage / Q000633:toxicity*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
chemical_list: C111835:CCL2 protein, human; C475829:CXCL1 protein, human; D018932:Chemokine CCL2; D054360:Chemokine CXCL1; D019743:Chemokines, CXC; D016207:Cytokines; D036341:Intercellular Signaling Peptides and Proteins; D015850:Interleukin-6; D016209:Interleukin-8; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D009538:Nicotine