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蜂毒磷脂酶 A2 通过 CD206 甘露糖受体缓解屋尘螨诱导的特应性皮炎样皮肤损伤。

Bee Venom Phospholipase A2 Alleviate House Dust Mite-Induced Atopic Dermatitis-Like Skin Lesions by the CD206 Mannose Receptor.

机构信息

Department of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, 26 kyungheedae-ro, dongdaemoon-ku, Seoul 02447, Korea.

出版信息

Toxins (Basel). 2018 Apr 2;10(4):146. doi: 10.3390/toxins10040146.

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 ( 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.

摘要

特应性皮炎(AD)是一种慢性炎症性皮肤病,其特征为剧烈瘙痒、红斑和湿疹样斑块。我们之前曾报道过,来源于蜂毒的磷脂酶 A2(PLA2)可减轻二硝基氯苯(DNCB)和屋尘螨提取物(DFE)诱导的小鼠模型中的 AD 样皮肤损伤。然而,PLA2 在特应性皮炎中的作用机制尚不清楚。在这项研究中,我们发现 PLA2 治疗可抑制由 DFE 和 DNCB 诱导的 AD 模型中耳朵的表皮厚度、血清免疫球蛋白 E(IgE)和细胞因子水平、巨噬细胞和肥大细胞浸润。相比之下,在接触 DFE 和 DNCB 的耳朵中,CD206 甘露糖受体缺陷型小鼠的这些作用被消除。这些数据表明,bvPLA2 通过与 CD206 相互作用来缓解特应性皮肤炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd4/5923312/3f85213dd3d5/toxins-10-00146-g001.jpg

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