title: Side-stream cigarette smoke accentuates immunomodulation during murine AIDS.
abstract: Side-stream cigarette smoke has become a hotly debated social, political, and scientific health and safety issue for nonsmokers. The harmful influences of side-stream cigarette smoke on human health are its adverse effects on the immune system, especially when already compromised by other agents. Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by human immunodeficiency virus (HIV). To facilitate studies, murine AIDS was induced in C57BL/6 mice by LP-BM5 murine leukemia virus infection, which mimics human AIDS. After 2 weeks of retroviral infection, the mice were exposed to side-stream cigarette smoke for 30 min, 5 days/week for 12 weeks using a side-stream cigarette smoke exposure system. Murine retrovirus infection reduced the in vitro proliferation of T lymphocytes stimulated by concanavalin A, increased the release of pro-inflammatory cytokine interleukin-6 (IL-6) tumor necrosis factor-alpha (TNF-alpha), increased the hepatic lipid peroxidation and decreased the alpha-tocopherol levels in liver, lung and heart. Concomitant side-stream cigarette smoke exposure for 12 weeks further inhibited the proliferation of T cells, increased the release of TNF-alpha, IL-6 cytokines and enhanced the hepatic lipid peroxidation from retrovirus infected mice. The loss of alpha-tocopherol was also further enhanced by side-stream cigarette smoke exposure during retrovirus infection. Our conclusions are that side-stream cigarette smoke induced increasing oxidative stress, reducing nutrient concentrations and suppressing immune function could make mice with murine AIDS more susceptible to opportunistic infections, potentially accelerating murine AIDS progression. Thus, the reduction of side-stream cigarette smoke exposure is an important health issue in AIDS patients to improve the quality and quantity of their lives.
authors.affiliation: Health Promotion Science Division, College of Public Health, The University of Arizona Health Science Center, Tuscon 85724, USA.
authors.forename: Jin
authors.initials: J
authors.lastname: Zhang
authors.forename: En-Jie
authors.initials: EJ
authors.lastname: Du Ester
authors.forename: Ronald Ross
authors.initials: RR
authors.lastname: Watson
mesh_terms: D000818:Animals; D016207:Cytokines / Q000096:biosynthesis; D015536:Down-Regulation / Q000276:immunology; D005260:Female; D009052:Leukemia Virus, Murine / Q000276:immunology*; D007942:Leukemia, Experimental / Q000276:immunology; D008054:Lipid Peroxides / Q000378:metabolism; D008213:Lymphocyte Activation; D051379:Mice; D008810:Mice, Inbred C57BL; D016183:Murine Acquired Immunodeficiency Syndrome / Q000276:immunology*; D018384:Oxidative Stress / Q000276:immunology; D013154:Spleen / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D014412:Tumor Virus Infections / Q000276:immunology; D015854:Up-Regulation / Q000276:immunology; D024502:alpha-Tocopherol / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D016207:Cytokines; D008054:Lipid Peroxides; D014028:Tobacco Smoke Pollution; D024502:alpha-Tocopherol