Systemic and stratum corneum biomarkers of severity in infant atopic dermatitis include markers of innate and T helper cell-related immunity and angiogenesis.

Systemic and stratum corneum biomarkers of severity in infant atopic dermatitis include markers of innate and T helper cell-related immunity and angiogenesis.
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DOI:
10.1111/bjd.17088
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发表时间:
2019-03
期刊:
The British journal of dermatology
影响因子:
--
通讯作者:
Irvine AD
Irvine AD
中科院分区:
其他
文献类型:
--
作者:
McAleer MA;Jakasa I;Hurault G;Sarvari P;McLean WHI;Tanaka RJ;Kezic S;Irvine AD

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特应性皮炎(AD)的生物标志物在很大程度上缺乏,特别是在婴儿AD中。迄今为止,这些研究主要集中在血清细胞因子上,很少涉及皮肤中的非侵入性生物标志物。我们的目的是探索从婴儿皮肤的非侵入性取样中获得的生物标志物。我们将这些与血浆生物标志物和皮肤屏障的结构和功能测量进行了比较。我们招募了100名首次出现阿尔茨海默病的婴儿,他们未接受局部或全身抗炎治疗,以及20名健康儿童。我们通过胶带剥离角质层(SC)取样临床未受影响的皮肤。SC和血浆中检测多种细胞因子、趋化因子和天然保湿因子。我们记录疾病严重程度和皮肤屏障功能。19个SC和12个血浆生物标志物在健康皮肤和AD皮肤之间显示显著差异。一些生物标志物在SC和血浆中是共同的,而另一些则是室特异性的。已确定的AD严重程度的生物标志物包括T辅助2‐倾斜标志物[白细胞介素(IL)‐13,CCL17, CCL22, IL‐5];先天激活(IL‐18,IL‐1α, IL‐1 β, CXCL8)和血管生成(Flt‐1,血管内皮生长因子)的标志物;和其他(可溶性细胞间粘附分子- 1,可溶性血管细胞粘附分子- 1,IL - 16, IL - 17A)。我们确定了阿尔茨海默病的临床相关生物标志物,包括易于在婴儿中取样和分型的新标志物。这些标志物可以提供客观的疾病严重程度评估,并建议新的治疗靶点,或AD的反应测量靶点。未来的研究将需要确定这些在早期AD中看到的生物标志物是否可以预测疾病结局或合并症。关于这个话题我们已经知道了什么?特应性皮炎是一种临床异质性疾病,临床表现多样,发病机制复杂。严重程度的系统生物标志物已在成人中确定,但在儿童中尚未明确定义。迄今为止,来自皮肤隔室的生物标志物是基于活组织检查。这项研究补充了什么?无创取样可以检测AD皮肤中临床相关的生物标志物。这些生物标志物可能对疾病分层有用,并为婴儿AD的发病机制提供见解。先天性免疫激活在婴儿AD的表皮中起重要作用。翻译的信息是什么?非侵入性生物标志物可以对婴儿阿尔茨海默病产生重要的见解。他们发现先天激活、辅助性T 2途径和血管生成是这种情况下的重要途径。回复这篇文章链接评论:Hijnen。中华皮肤科杂志2019;180:455 - 456。在线提供简单的语言摘要
Biomarkers of atopic dermatitis (AD) are largely lacking, especially in infant AD. Those that have been examined to date have focused mostly on serum cytokines, with few on noninvasive biomarkers in the skin. We aimed to explore biomarkers obtainable from noninvasive sampling of infant skin. We compared these with plasma biomarkers and structural and functional measures of the skin barrier. We recruited 100 infants at first presentation with AD, who were treatment naive to topical or systemic anti‐inflammatory therapies, and 20 healthy children. We sampled clinically unaffected skin by tape stripping the stratum corneum (SC). Multiple cytokines and chemokines and natural moisturizing factor were measured in the SC and plasma. We recorded disease severity and skin barrier function. Nineteen SC and 12 plasma biomarkers showed significant differences between healthy and AD skin. Some biomarkers were common to both the SC and plasma, and others were compartment specific. Identified biomarkers of AD severity included T helper 2‐skewed markers [interleukin (IL)‐13, CCL17, CCL22, IL‐5]; markers of innate activation (IL‐18, IL‐1α, IL1β, CXCL8) and angiogenesis (Flt‐1, vascular endothelial growth factor); and others (soluble intercellular adhesion molecule‐1, soluble vascular cell adhesion molecule‐1, IL‐16, IL‐17A). We identified clinically relevant biomarkers of AD, including novel markers, easily sampled and typed in infants. These markers may provide objective assessment of disease severity and suggest new therapeutic targets, or response measurement targets for AD. Future studies will be required to determine whether these biomarkers, seen in very early AD, can predict disease outcomes or comorbidities. What's already known about this topic? Atopic dermatitis is a clinically heterogeneous condition with multiple clinical manifestations and a complex pathogenesis. Systemic biomarkers of severity have been identified in adults, but are less well defined in children. Biomarkers from the skin compartment have been based on biopsies to date. What does this study add? Noninvasive sampling can detect clinically relevant biomarkers in AD skin. These biomarkers may be useful for disease stratification, and provide insights into the pathogenesis of infant AD. Innate immune activation is important in the epidermis in infantile AD. What is the translational message? Noninvasive biomarkers can yield significant insights into infantile AD. They identify innate activation, the T helper 2 pathway and angiogenesis as important pathways in this condition. Respond to this article Linked Comment: Hijnen. Br J Dermatol 2019; 180:455–456. Plain language summary available online
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