| Surfactant protein D inhibits mite-induced alveolar macrophage and dendritic cell activations through TLR signalling and DC-SIGN expression. | |
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MedLine Citation:
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PMID: 20205699 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Surfactant protein D (SP-D), a secreted pattern recognition molecule associated with pulmonary innate immunity, has been shown to mediate the clearance of pathogens in multiple ways. However, how SP-D interacts with alveolar macrophages (AMs) and dendritic cells (DCs) during allergen exposure remains unclear. OBJECTIVE: This study was performed to characterize the immunomodulatory effects of SP-D on mite allergen (Dermatophagoides pteronyssinus, Der p)-induced inflammatory signalling in AMs and DCs. METHODS: Murine AM, alveolar macrophage cell line derived from BALB/c mice (MH-S cells), and human monocyte-derived dendritic cells (MDDC) were used as model systems. The production of nitric oxide (NO) and TNF-alpha, expression of surface Toll-like receptors (TLRs), and expression of the C-type lectin receptor known as dendritic cell (DC)-specific ICAM-grabbing non-integrin (DC-SIGN) were measured as a function of pretreatment with SP-D and subsequent exposure to Der p. Der p-dependent cellular activations that were modified by SP-D in these model systems were then identified. RESULTS: Pretreatment of MH-S cells with SP-D reduced Der p-dependent production of NO, TNF-alpha, and the downstream activations of IL-1 receptor-associated kinase, mitogen activated protein kinase (MAPK) kinase, and nuclear factor-kappaB. SP-D interacted with CD14 such that CD14 binding to Der p was inhibited and Der p-induced signalling via TLRs was blocked. DC-SIGN expression was suppressed by Der p in MH-S and MDDC; this down-regulation of DC-SIGN expression was prevented by pretreatment with SP-D. CONCLUSIONS: These results indicated that the inhibition of Der p-induced activation of MH-S and MDDC by SP-D is mediated through suppression of the CD14/TLR signalling pathway and maintenance of DC-SIGN expression, which may protect allergen-induced airway inflammation. |
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Authors:
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C-F Liu; M Rivere; H-J Huang; G Puzo; J-Y Wang |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
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 Jan |
Date Detail:
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Created Date: 2010-03-08 Completed Date: 2010-06-18 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: 111-22 Citation Subset: IM |
Affiliation:
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Department of Pediatrics, Division of Clinical Immunology and Allergy, Institute of Basic Medical Sciences, College of Medicine, National Cheng-Kung University, Tainan, Taiwan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Allergens
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immunology Animals Antigens, Dermatophagoides / immunology Cell Adhesion Molecules / biosynthesis, metabolism* Cells, Cultured Dendritic Cells / immunology* Dermatophagoides pteronyssinus / immunology* Down-Regulation / drug effects Humans Lectins, C-Type / biosynthesis, metabolism* Macrophages, Alveolar / immunology* Mice Mice, Inbred BALB C Nitric Oxide / biosynthesis Pulmonary Surfactant-Associated Protein D / metabolism*, pharmacology Receptors, Cell Surface / biosynthesis, metabolism* Recombinant Proteins / pharmacology Signal Transduction Toll-Like Receptors / metabolism* Tumor Necrosis Factor-alpha / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Allergens; 0/Antigens, Dermatophagoides; 0/Cell Adhesion Molecules; 0/DC-specific ICAM-3 grabbing nonintegrin; 0/Lectins, C-Type; 0/Pulmonary Surfactant-Associated Protein D; 0/Receptors, Cell Surface; 0/Recombinant Proteins; 0/Toll-Like Receptors; 0/Tumor Necrosis Factor-alpha; 10102-43-9/Nitric Oxide |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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