Source:http://linkedlifedata.com/resource/pubmed/id/18941201
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
9
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| pubmed:dateCreated |
2008-10-22
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| pubmed:abstractText |
IL-17 is a pivotal proinflammatory molecule in asthmatics. However, the cellular source of IL-17 in asthma has not been identified to date. In this study, we report that macrophages rather than Th17 cells are the main producer of IL-17 in allergic inflammation related to asthma. After OVA challenge in a mouse model mimicking allergic asthma, the increased IL-17(+) cells in the lung were mainly CD11b(+)F4/80(+) macrophages, instead of T cells or others. Importantly, IL-17(+) alveolar macrophages (AMs), but not IL-17(+) interstitial macrophages, were significantly increased after allergen challenge. The increase of IL-17(+) AMs was not due to the influx of IL-17(+) macrophages from circulation or other tissues, but ascribed to the activation of AMs by mediator(s) secreted by IgE/OVA-activated mast cells. Depleting alveolar macrophages or neutralizing IL-17 prevented the initiation of OVA-induced asthma-related inflammation by inhibiting the increase of inflammatory cells and inflammatory factors in bronchoalveolar lavage fluid. Th2 cytokine IL-10 could down-regulate IL-17 expression in alveolar macrophages. The increased IL-17 and the decreased IL-10 in bronchoalveolar lavage fluid were further confirmed in asthmatic patients. These findings suggest that IL-17 is mainly produced by macrophages but not Th17 cells in allergic inflammation related to asthma. Mast cell-released mediators up-regulate the expression of IL-17 by macrophages, whereas IL-10 down-regulates IL-17 expression.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Nov
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| pubmed:issn |
1550-6606
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
1
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| pubmed:volume |
181
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
6117-24
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| pubmed:meshHeading |
pubmed-meshheading:18941201-Acute Disease,
pubmed-meshheading:18941201-Adult,
pubmed-meshheading:18941201-Animals,
pubmed-meshheading:18941201-Antigens, CD11b,
pubmed-meshheading:18941201-Antigens, Differentiation,
pubmed-meshheading:18941201-Asthma,
pubmed-meshheading:18941201-Cells, Cultured,
pubmed-meshheading:18941201-Disease Models, Animal,
pubmed-meshheading:18941201-Female,
pubmed-meshheading:18941201-Humans,
pubmed-meshheading:18941201-Hypersensitivity,
pubmed-meshheading:18941201-Immunity, Cellular,
pubmed-meshheading:18941201-Inflammation,
pubmed-meshheading:18941201-Interleukin-17,
pubmed-meshheading:18941201-Lung,
pubmed-meshheading:18941201-Macrophages, Alveolar,
pubmed-meshheading:18941201-Mice,
pubmed-meshheading:18941201-Mice, Inbred BALB C,
pubmed-meshheading:18941201-Middle Aged,
pubmed-meshheading:18941201-Up-Regulation
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| pubmed:year |
2008
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| pubmed:articleTitle |
IL-17-producing alveolar macrophages mediate allergic lung inflammation related to asthma.
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| pubmed:affiliation |
Department of Biochemistry & Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, The People's Republic of China.
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| pubmed:publicationType |
Journal Article
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