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Clinical & Experimental Allergy

Surfactant protein D inhibits mite-induced alveolar macrophage and dendritic cell activations through TLR signalling and DC-SIGN expression

Authors

  • C-F Liu,

    1. Department of Pediatrics, Division of Clinical Immunology and Allergy, Institute of Basic Medical Sciences, College of Medicine, National Cheng-Kung University, Tainan, Taiwan
    2. Department of Pediatrics, Institute of Microbiology and Immunology, College of Medicine, National Cheng-Kung University, Tainan, Taiwan
    3. Department of Immunology, University Paul Sabatier, Toulouse, France
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  • M. Rivere,

    1. Institut de Pharmacologie et de Biologie Structurale, Toulouse Cedex, France
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  • H-J Huang,

    1. Department of Pediatrics, Institute of Microbiology and Immunology, College of Medicine, National Cheng-Kung University, Tainan, Taiwan
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  • G. Puzo,

    1. Institut de Pharmacologie et de Biologie Structurale, Toulouse Cedex, France
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  • J-Y Wang

    1. Department of Pediatrics, Division of Clinical Immunology and Allergy, Institute of Basic Medical Sciences, College of Medicine, National Cheng-Kung University, Tainan, Taiwan
    2. Department of Pediatrics, Institute of Microbiology and Immunology, College of Medicine, National Cheng-Kung University, Tainan, Taiwan
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Correspondence:
Jiu-Yao Wang, Department of Pediatrics, Division of Clinical Immunology and Allergy, Institute of Basic Medical Sciences, College of Medicine, National Cheng-Kung University, No. 138, Sheng-Li Road, Tainan 70101, Taiwan.
E-mail: a122@mail.ncku.edu.tw

Summary

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-α, 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-α, and the downstream activations of IL-1 receptor-associated kinase, mitogen activated protein kinase (MAPK) kinase, and nuclear factor-κB. 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.

Cite this as: C-F Liu, M. Rivere, H-J Huang, G. Puzo and J-Y Wang, Clinical & Experimental Allergy, 2010 (40) 111–122.

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