| Inhibition of immunological function mediated DNA damage of alveolar macrophages caused by cigarette smoke in mice. | |
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MedLine Citation:
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PMID: 19922407 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Exposure to cigarette smoke impairs the pulmonary immune system, including alveolar macrophage function, although the mechanisms by which this occurs are not fully elucidated. This study investigates the effect of cigarette smoke exposure on the antigen-presenting activity of alveolar macrophages, which is required for antigen-specific response to T cells. C57BL/6 mice were exposed to cigarette smoke for 10 days using a Hamburg II smoking machine, and alveolar macrophages were obtained by bronchoalveolar lavage. The antigen-presenting activity of alveolar macrophages was significantly inhibited in mice exposed to cigarette smoke compared with mice not exposed to cigarette smoke. Major histocompatibility complex class II cell surface molecule-positive cells, B7-1 molecule-positive cells, and interleukin-1beta messenger RNA gene expression in alveolar macrophages were significantly decreased in mice exposed to cigarette smoke compared with mice not exposed to cigarette smoke. In contrast, DNA damage and generation of superoxide and hydrogen peroxide in alveolar macrophages were significantly increased by cigarette smoke exposure. These results suggest that inhibition of the antigen-presenting activity of alveolar macrophages may result from decreased expression of major histocompatibility complex class II and B7-1 molecules and interleukin-1beta messenger RNA gene expression following cigarette smoke exposure. Furthermore, inhibition of antigen presentation in alveolar macrophage may result from DNA damage induced by excessive amounts of reactive oxygen species being generated by alveolar macrophages following cigarette smoke exposure. These findings suggest that cigarette smoke impairs the immunological function of alveolar macrophages and, as a result, increases the risk for pulmonary infection. |
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Authors:
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Takahiro Ishida; Yuriko Hirono; Kenichi Yoshikawa; Yoshimi Hutei; Mayuko Miyagawa; Ikuyo Sakaguchi; Kent E Pinkerton; Minoru Takeuchi |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Inhalation toxicology Volume: 21 ISSN: 1091-7691 ISO Abbreviation: Inhal Toxicol Publication Date: 2009 Dec |
Date Detail:
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Created Date: 2009-11-20 Completed Date: 2010-01-26 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8910739 Medline TA: Inhal Toxicol Country: England |
Other Details:
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Languages: eng Pagination: 1229-35 Citation Subset: IM |
Affiliation:
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Department of Biotechnology, Faculty of Engineering, Kyoto Sangyo University, Kyoto 603-8555, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antigen Presentation / drug effects* Antigens, CD80 / genetics Carboxyhemoglobin / metabolism Cells, Cultured DNA Damage* Down-Regulation Female Histocompatibility Antigens Class II / genetics Hydrogen Peroxide / metabolism Inhalation Exposure Interleukin-1beta / genetics Macrophages, Alveolar / drug effects*, immunology, pathology Mice Mice, Inbred C57BL Oxidative Stress / drug effects* RNA, Messenger / metabolism Smoke / adverse effects* Smoking / adverse effects* Superoxides / metabolism Time Factors Tobacco / toxicity* |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD80; 0/Histocompatibility Antigens Class II; 0/Interleukin-1beta; 0/RNA, Messenger; 0/Smoke; 11062-77-4/Superoxides; 7722-84-1/Hydrogen Peroxide; 9061-29-4/Carboxyhemoglobin |
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