Abstract |
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by highly pruritic, erythematous, and eczematous skin plaques. We previously reported that phospholipase A2 (PLA2) derived from bee venom alleviates AD-like skin lesions induced by 2,4-dinitrochlorobenzene ( DNCB) and house dust mite extract (Dermatophagoides farinae extract, DFE) in a murine model. However, the underlying mechanisms of PLA2 action in actopic dermatitis remain unclear. In this study, we showed that PLA2 treatment inhibited epidermal thickness, serum immunoglobulin E ( IgE) and cytokine levels, macrophage and mast cell infiltration in the ear of an AD model induced by DFE and DNCB. In contrast, these effects were abrogated in CD206 mannose receptor-deficient mice exposed to DFE and DNCB in the ear. These data suggest that bvPLA2 alleviates atopic skin inflammation via interaction with CD206.
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Authors | Dasom Shin, Won Choi, Hyunsu Bae |
Journal | Toxins
(Toxins (Basel))
Vol. 10
Issue 4
(04 02 2018)
ISSN: 2072-6651 [Electronic] Switzerland |
PMID | 29614845
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Anti-Inflammatory Agents
- Bee Venoms
- Cytokines
- Dinitrochlorobenzene
- Lectins, C-Type
- Mannose Receptor
- Mannose-Binding Lectins
- Receptors, Cell Surface
- Immunoglobulin E
- Phospholipases A2
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Topics |
- Animals
- Anti-Inflammatory Agents
(pharmacology, therapeutic use)
- Bee Venoms
(enzymology)
- Cytokines
(blood)
- Dermatitis, Atopic
(drug therapy, metabolism)
- Dinitrochlorobenzene
- Immunoglobulin E
(blood)
- Lectins, C-Type
(genetics, metabolism)
- Male
- Mannose Receptor
- Mannose-Binding Lectins
(genetics, metabolism)
- Mice, Inbred C57BL
- Mice, Knockout
- Phospholipases A2
(pharmacology, therapeutic use)
- Pyroglyphidae
- Receptors, Cell Surface
(genetics, metabolism)
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