| Inhibiting or blocking LIGHT, a TNF superfamily member, for treating airway remodeling. | |
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MedLine Citation:
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PMID: 21955232 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Evaluation of: Doherty TA, Soroosh P, Khorram N et al. The tumor necrosis factor family member LIGHT is a target for asthmatic airway remodeling. Nat. Med. 17, 596-603 (2011). Individuals with chronic asthma demonstrate a progressive decline in lung function that is thought to be due to structural remodeling of the airways, characterized by subepithelial fibrosis and smooth muscle hyperplasia. Here we report on a recent publication showing that the tumor necrosis factor family member LIGHT is expressed on lung inflammatory cells after allergen exposure. Pharmacological inhibition of LIGHT using a fusion protein between the IgG Fc domain and lymphotoxin-β-receptor reduces lung fibrosis, smooth muscle hyperplasia and airway hyperresponsiveness in mouse models of chronic asthma, despite having little effect on airway eosinophilia. LIGHT-deficient mice also show a similar impairment in fibrosis and smooth muscle accumulation. Blockade of LIGHT suppresses expression of lung TGF-β and IL-13, cytokines implicated in remodeling in humans, whereas exogenous administration of LIGHT to the airways induces fibrosis and smooth muscle hyperplasia; thus, LIGHT may be targeted to prevent asthma-related airway remodeling. |
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Authors:
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Mario Cazzola; Maria Gabriella Matera |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Expert review of respiratory medicine Volume: 5 ISSN: 1747-6356 ISO Abbreviation: Expert Rev Respir Med Publication Date: 2011 Oct |
Date Detail:
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Created Date: 2011-09-29 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101278196 Medline TA: Expert Rev Respir Med Country: England |
Other Details:
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Languages: eng Pagination: 623-5 Citation Subset: IM |
Affiliation:
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Unit of Respiratory Clinical Pharmacology, Department of Internal Medicine, University of Rome, Rome, Italy. mario.cazzola@uniroma2.it. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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