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单纯疱疹病毒 1 蛋白可诱导特应性皮炎样小鼠模型的皮肤炎症。

Herpes simplex virus 1 proteins can induce skin inflammation in an atopic dermatitis-like mouse model.

机构信息

Department of Dermatology and Allergy, University Hospital Bonn, Bonn, Germany.

Immunology & Environment, Life and Medical Sciences (LIMES) Institute, University of Bonn, Bonn, Germany.

出版信息

Exp Dermatol. 2021 Nov;30(11):1699-1704. doi: 10.1111/exd.14327. Epub 2021 Mar 22.

Abstract

Herpes simplex virus type 1 (HSV-1) can induce in certain individuals with atopic dermatitis (AD) severe cutaneous infections that can spread throughout the entire body, a condition named as AD complicated by eczema herpeticum (ADEH). It has been recently found that ADEH patients can produce specific IgE against HSV-1 proteins, which may contribute to lower protection against HSV-1. However, little is known about the capacity of these HSV-1 proteins to produce an inflammatory response at the skin level. In this study, using a mouse model of AD-like dermatitis, three HSV-1 proteins (glycoprotein D -gD-, glycoprotein B -gB- and VP22) were applied on tape-stripped back skin mice in three exposures periods. Ovalbumin (OVA) and 0.9% NaCl were used as positive and negative controls, respectively. Skin samples were obtained for analysis of specific cell components of skin infiltration. The results showed that the viral protein gD induced a statistically significant increase in the number of dermal infiltrating CD3+, CD4+ cells and mast cells compared with the negative control group. gD was also able to induce epidermal thickening and epidermal infiltration of T cells closely related to the one produced in mice sensitized with OVA. However, VP22 and gB contributed to a lesser extent to skin inflammation. These results showed that proteins from HSV-1, especially gD, can have per se an important T cell and mast cell-driven inflammatory potential at the skin level.

摘要

单纯疱疹病毒 1 型(HSV-1)可在特应性皮炎(AD)患者中引发严重的皮肤感染,甚至可扩散至全身,这种情况被称为伴有疱疹样湿疹(ADEH)的 AD。最近发现,ADEH 患者可针对 HSV-1 蛋白产生特异性 IgE,这可能导致对 HSV-1 的保护作用降低。然而,目前对于这些 HSV-1 蛋白在皮肤水平产生炎症反应的能力知之甚少。在这项研究中,使用类似于 AD 的皮炎小鼠模型,在三个暴露期内将三种 HSV-1 蛋白(糖蛋白 D-gD、糖蛋白 B-gB 和 VP22)应用于胶带剥离的背部皮肤小鼠上。卵清蛋白(OVA)和 0.9%NaCl 分别用作阳性和阴性对照。获取皮肤样本以分析皮肤浸润的特定细胞成分。结果表明,与阴性对照组相比,病毒蛋白 gD 诱导真皮浸润 CD3+、CD4+细胞和肥大细胞的数量呈统计学显著增加。gD 还能够诱导与 OVA 致敏小鼠产生的类似的表皮增厚和表皮 T 细胞浸润。然而,VP22 和 gB 的作用程度较小。这些结果表明,HSV-1 的蛋白,特别是 gD,本身在皮肤水平具有重要的 T 细胞和肥大细胞驱动的炎症潜力。

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