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Surfactant protein D inhibits mite-induced alveolar macrophage and dendritic cell activations through TLR signalling
1Department of Pediatrics, Division of Clinical Immunology and Allergy, Institute of Basic Medical Sciences, College of Medicine, National Cheng-Kung University, Tainan, Taiwan.
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.
Insights
Surfactant protein D (SP-D) modulates immune responses to mite allergens by inhibiting inflammatory signaling in macrophages and dendritic cells. SP-D maintains DC-SIGN expression, potentially protecting against airway inflammation.
Area of Science:
- Immunology
- Pulmonary Medicine
- Innate Immunity
Background:
- Surfactant protein D (SP-D) is a key molecule in pulmonary innate immunity involved in pathogen clearance.
- The interaction between SP-D and immune cells like alveolar macrophages (AMs) and dendritic cells (DCs) during allergen exposure is not well understood.
Purpose of the Study:
- To investigate the immunomodulatory effects of SP-D on mite allergen (Der p)-induced inflammatory signaling in AMs and DCs.
- To characterize how SP-D influences key immune pathways and cell surface receptors.
Main Methods:
- Utilized murine AMs (MH-S cells) and human monocyte-derived dendritic cells (MDDCs) as model systems.
- Measured nitric oxide (NO), TNF-alpha, Toll-like receptors (TLRs), and DC-SIGN expression following SP-D pretreatment and Der p exposure.
Main Results:
- SP-D pretreatment reduced Der p-induced production of NO and TNF-alpha, and downstream signaling via MAPK and NF-kappaB.
- SP-D inhibited Der p binding to CD14, blocking TLR-mediated signaling.
- SP-D prevented the suppression of DC-SIGN expression by Der p in both cell types.
Conclusions:
- SP-D inhibits Der p-induced activation of AMs and MDDCs by suppressing the CD14/TLR signaling pathway.
- SP-D maintains DC-SIGN expression, suggesting a protective role against allergen-induced airway inflammation.
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