| SP-D and regulation of the pulmonary innate immune system in allergic airway changes. | |
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MedLine Citation:
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PMID: 20447075 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The airway mucosal surfaces are constantly exposed to inhaled particles that can be potentially toxic, infectious or allergenic and should elicit inflammatory changes. The proximal and distal air spaces, however, are normally infection and inflammation free due to a specialized interplay between cellular and molecular components of the pulmonary innate immune system. Surfactant protein D (SP-D) is an epithelial-cell-derived immune modulator that belongs to the small family of structurally related Ca(2+)-dependent C-type collagen-like lectins. While collectins can be detected in mucosal surfaces of various organs, SP-A and SP-D (the 'lung collectins') are constitutively expressed in the lung at high concentrations. Both proteins are considered important players of the pulmonary immune responses. Under normal conditions however, SP-A-/- mice display no pathological features in the lung. SP-D-/- mice, on the other hand, show chronic inflammatory alterations indicating a special importance of this molecule in regulating immune homeostasis and the function of the innate immune cells. Recent studies in our laboratory and others implied significant associations between changes in SP-D levels and the presence of airway inflammation both in animal models and patients raising a potential usefulness of this molecule as a disease biomarker. Research on wild-type and mutant recombinant molecules in vivo and in vitro showed that SP-D binds carbohydrates, lipids and nucleic acids with a broad spectrum specificity and initiates phagocytosis of inhaled pathogens as well as apoptotic cells. Investigations on gene-deficient and conditional over expressor mice in addition, provided evidence that SP-D directly modulates macrophage and dendritic cell function as well as T cell-dependent inflammatory events. Thus, SP-D has a unique, dual functional capacity to induce pathogen elimination on the one hand and control of pro-inflammatory mechanisms on the other, suggesting a potential suitability for therapeutic prevention and treatment of chronic airway inflammation without compromising the host defence function of the airways. This paper will review recent findings on the mechanisms of immune-protective function of SP-D in the lung. |
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Authors:
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L R Forbes; A Haczku |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology Volume: 40 ISSN: 1365-2222 ISO Abbreviation: Clin. Exp. Allergy Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-05-07 Completed Date: 2010-08-24 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8906443 Medline TA: Clin Exp Allergy Country: England |
Other Details:
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Languages: eng Pagination: 547-62 Citation Subset: IM |
Affiliation:
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Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Gene Expression Regulation* Humans Immunity, Innate / immunology* Lung / immunology* Mice Pulmonary Surfactant-Associated Protein D / genetics, immunology*, metabolism Respiratory Hypersensitivity / immunology* |
| Grant Support | |
ID/Acronym/Agency:
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R01AI055593/AI/NIAID NIH HHS; R01HL076646/HL/NHLBI NIH HHS; RC1ES018505/ES/NIEHS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Pulmonary Surfactant-Associated Protein D |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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