Source:http://linkedlifedata.com/resource/pubmed/id/19502389
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2010-3-15
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| pubmed:abstractText |
The objective of this study was to characterize the impact of cigarette smoke exposure on lung immune and inflammatory processes. BALB/c and C57BL/6 mice were exposed to cigarette smoke for 4 days (acute) or at least 5 weeks (prolonged). Both mouse strains manifested an inflammatory response after acute smoke exposure, characterized by an influx of neutrophils and mononuclear cells. Multiplex analysis revealed a greater than twofold increase of the cytokines IL-1alpha, -5, -6, and -18, as well as the chemokines monocyte chemotactic protein-1 and -3, macrophage inflammatory protein-1alpha, -beta, and -gamma, -2, -3beta, macrophage defined chemokine, granulocyte chemotactic protein-2, and interferon-gamma-inducible protein-10. In BALB/c mice, neutrophilia persisted after prolonged exposure, whereas C57BL/6 showed evidence of attenuated neutrophilia both in the bronchoalveolar lavage and the lungs. In both mouse strains, cigarette smoke exposure was associated with an expansion of mature (CD11c(hi)/major histocompatibility complex class II(hi)) myeloid dendritic cells; we observed no changes in plasmacytoid dendritic cells. Lymphocytes in the lungs displayed an activated phenotype that persisted for CD4 T cells only after prolonged exposure. In BALB/c mice, T cells acquired T helper (Th) 1 and Th2 effector function after 5 weeks of smoke exposure, whereas, in C57BL/6 mice, neither Th1 nor Th2 cells were detected. In both mouse strains, cigarette smoke exposure led to an accumulation of FoxP3+ T regulatory cells in the lungs. Studies in RAG1 knockout mice suggest that these regulatory cells may participate in controlling smoke-induced inflammation. Acute and prolonged cigarette smoke exposure was associated with inflammation, activation of the adaptive immune system, and expansion of T regulatory cells in the lungs.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
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| pubmed:issn |
1535-4989
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
42
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
394-403
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| pubmed:meshHeading |
pubmed-meshheading:19502389-Adaptive Immunity,
pubmed-meshheading:19502389-Animals,
pubmed-meshheading:19502389-Antigens, CD11c,
pubmed-meshheading:19502389-Bronchoalveolar Lavage,
pubmed-meshheading:19502389-Cytokines,
pubmed-meshheading:19502389-Dendritic Cells,
pubmed-meshheading:19502389-Female,
pubmed-meshheading:19502389-Homeodomain Proteins,
pubmed-meshheading:19502389-Humans,
pubmed-meshheading:19502389-Immunity, Innate,
pubmed-meshheading:19502389-Lung,
pubmed-meshheading:19502389-Mice,
pubmed-meshheading:19502389-Mice, Inbred BALB C,
pubmed-meshheading:19502389-Mice, Knockout,
pubmed-meshheading:19502389-Myeloid Cells,
pubmed-meshheading:19502389-Neutrophil Infiltration,
pubmed-meshheading:19502389-Neutrophils,
pubmed-meshheading:19502389-Pneumonia,
pubmed-meshheading:19502389-Smoking,
pubmed-meshheading:19502389-T-Lymphocytes, Regulatory,
pubmed-meshheading:19502389-Th1 Cells,
pubmed-meshheading:19502389-Th2 Cells,
pubmed-meshheading:19502389-Time Factors
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| pubmed:year |
2010
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| pubmed:articleTitle |
Innate immune processes are sufficient for driving cigarette smoke-induced inflammation in mice.
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| pubmed:affiliation |
Department of Pathology and Molecular Medicine, McMaster University, 1200 Main Street West Hamilton, ON L8N3Z5, Canada.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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