| Anti-inflammatory effects of the neurotransmitter agonist Honokiol in a mouse model of allergic asthma. | |
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MedLine Citation:
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PMID: 20889543 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Chronic airway inflammation is a hallmark of asthma, an immune-based disease with great societal impact. Honokiol (HNK), a phenolic neurotransmitter receptor (γ-aminobutyric acid type A) agonist purified from magnolia, has anti-inflammatory properties, including stabilization of inflammation in experimentally induced arthritis. The present study tested the prediction that HNK could inhibit the chronic inflammatory component of allergic asthma. C57BL/6 mice sensitized to and challenged with OVA had increased airway hyperresponsiveness to methacholine challenge and eosinophilia compared with naive controls. HNK-treated mice showed a reduction in airway hyperresponsiveness as well as a significant decrease in lung eosinophilia. Histopathology studies revealed a marked drop in lung inflammation, goblet cell hyperplasia, and collagen deposition with HNK treatment. Ag recall responses from HNK-treated mice showed decreased proinflammatory cytokines in response to OVA, including TNF-α-, IL-6-, Th1-, and Th17-type cytokines, despite an increase in Th2-type cytokines. Regulatory cytokines IL-10 and TGF-β were also increased. Assessment of lung homogenates revealed a similar pattern of cytokines, with a noted increase in the number of FoxP3(+) cells in the lung. HNK was able to alter B and T lymphocyte cytokine secretion in a γ-aminobutyric acid type A-dependent manner. These results indicate that symptoms and pathology of asthma can be alleviated even in the presence of increased Th2 cytokines and that neurotransmitter agonists such as HNK have promise as a novel class of anti-inflammatory agents in the treatment of chronic asthma. |
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Authors:
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Melissa E Munroe; Thomas R Businga; Joel N Kline; Gail A Bishop |
Related Documents
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12668793 - T cell cytokine profiles in childhood asthma. 18721323 - Allergy and the lung. 22077983 - Evidence of a role for th17 cells in the breach of immune tolerance in arthritis. |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. Date: 2010-10-01 |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 185 ISSN: 1550-6606 ISO Abbreviation: J. Immunol. Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-10-21 Completed Date: 2010-11-12 Revised Date: 2011-11-01 |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 5586-97 Citation Subset: AIM; IM |
Affiliation:
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Department of Microbiology, University of Iowa, Iowa City, IA 52242, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anti-Inflammatory Agents / therapeutic use* Asthma / drug therapy*, immunology Biphenyl Compounds / therapeutic use* Cytokines / biosynthesis, immunology Disease Models, Animal Enzyme-Linked Immunosorbent Assay Eosinophilia / immunology Female Fluorescent Antibody Technique Hypersensitivity / complications, drug therapy* Lignans / therapeutic use* Lung / drug effects*, immunology, pathology Mice Mice, Inbred C57BL Th2 Cells / drug effects, immunology |
| Grant Support | |
ID/Acronym/Agency:
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AT003998/AT/NCCAM NIH HHS; R21 AT003998-01A2/AT/NCCAM NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Anti-Inflammatory Agents; 0/Biphenyl Compounds; 0/Cytokines; 0/Lignans; 35354-74-6/honokiol |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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