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特应性皮炎中瘙痒和疾病严重程度的生物标志物。

Biomarkers for itch and disease severity in atopic dermatitis.

作者信息

Lee Chih-Hung, Yu Hsin-Su

出版信息

Curr Probl Dermatol. 2011;41:136-148. doi: 10.1159/000323307. Epub 2011 May 12.

Abstract

Atopic dermatitis (AD) is a common allergic disease and constitutes a huge social and economic burden for the whole country. AD usually heralds other allergic diseases, such as asthma and allergic rhinitis. The pathogenesis of AD remains to be studied but generally includes abnormal skin barrier and aberrant cutaneous immune responses. Biomarkers are important in monitoring disease severity, prognosis and treatment responses. With the investigation and robust knowledge on AD pathophysiology, more and more biomarkers are being explored. Aberrant cutaneous inflammation is associated with Th2 polarization, chemokine upregulation in Langerhans cells and keratinocytes, IgE production by B cells, and degranulation of mast cells and eosinophils, subsequently leading to changes in the levels of cell-specific biomarkers in blood or urine. Furthermore, skin barrier abnormalities, including increased transepidermal water loss and decreased skin hydration, are biomarkers for severity and itch intensity in AD. Cross-talk between skin barrier abnormalities and aberrant immune responses is evidenced by epidermal abnormalities enhancing the release of keratinocyte-derived cytokines and chemokines, including CC chemokine ligand (CCL) 17, CCL27 and thymic stromal lymphopoietin, resulting in modulation of skin immune responses. The pathophysiology of itch in AD remains unclear. The subjective nature of itch makes biomarkers to estimate its intensity crucial in AD patients. Pruritus results from the activation of small nerve endings in the skin by noxious mediators, including neuropeptides, proinflammatory cytokines and prostaglandins, all of which might serve as potential biomarkers for itch. Recently, IL-31 and gastrin-releasing peptide have been reported to be involved in the development of itch, making the estimation of itch intensity a future reality. With the enormous amount of research in immunology, skin physiology and neurology in AD, more biomarkers in AD and its itch will be found in the near future.

摘要

特应性皮炎(AD)是一种常见的过敏性疾病,给整个国家带来了巨大的社会和经济负担。AD通常是其他过敏性疾病的先兆,如哮喘和过敏性鼻炎。AD的发病机制仍有待研究,但一般包括皮肤屏障异常和皮肤免疫反应异常。生物标志物在监测疾病严重程度、预后和治疗反应方面很重要。随着对AD病理生理学的深入研究和丰富认识,越来越多的生物标志物正在被探索。皮肤炎症异常与Th2极化、朗格汉斯细胞和角质形成细胞中趋化因子上调、B细胞产生IgE以及肥大细胞和嗜酸性粒细胞脱颗粒有关,随后导致血液或尿液中细胞特异性生物标志物水平发生变化。此外,皮肤屏障异常,包括经表皮水分流失增加和皮肤水合作用降低,是AD严重程度和瘙痒强度的生物标志物。皮肤屏障异常与免疫反应异常之间的相互作用表现为表皮异常增强角质形成细胞衍生的细胞因子和趋化因子的释放,包括CC趋化因子配体(CCL)17、CCL27和胸腺基质淋巴细胞生成素,从而调节皮肤免疫反应。AD中瘙痒的病理生理学仍不清楚。瘙痒的主观性使得评估其强度的生物标志物对AD患者至关重要。瘙痒是由包括神经肽、促炎细胞因子和前列腺素在内的有害介质激活皮肤中的小神经末梢引起的,所有这些都可能作为瘙痒的潜在生物标志物。最近,有报道称白细胞介素-31和胃泌素释放肽参与了瘙痒的发生,这使得评估瘙痒强度成为未来可能实现的事情。随着对AD免疫学、皮肤生理学和神经学的大量研究,在不久的将来会发现更多AD及其瘙痒相关的生物标志物。

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