Department of Pathology, Second Xiangya Hospital, Central South University Xiangya School of Medicine, 156 Renmin Road, Changsha, Hunan, P.R. China.
Int J Mol Med. 2010 Dec;26(6):779-85. doi: 10.3892/ijmm_00000525.
The skin, the conjunctivae, the airways and the digestive tract compose a huge vulnerable biological surface, which is exposed to the external environment. An allergen can often trigger an allergic reaction at a number of sites or result in an atopic march. However, the mechanism of atopic march remains unclear. Less attention has been paid to the connection between the primary site and the atopic site, because current knowledge is established directly against harmful factors. Allergic hypersensitivity manifests in parts of the human body far away from the allergen. Growing evidence suggests that the epithelial cells serve as the 'engine' which initiates an allergic reaction through the production of large quantities of cytokines, chemokines and growth factors. Because the epithelial cells cover the entire surface of the skin, the conjunctivae, the airways, and the digestive tract, and are positioned at the terminals of neurons and the blood supply, the connection between the primary site and the atopic site can not be easily understood by the current knowledge of anatomy and of the neuroendocrine immune network. What is the linkage between these huge vulnerable biologic surfaces? This article highlights selected frontiers in allergy research of atopic march, and focuses on recently attained insights into the cellular and molecular events of primary and atopic lesions in the allergy progress. Special attention is paid to the homogeneity of the cellular and molecular events on the huge vulnerable surface. Based on currently available data we conclude that the skin, conjunctivae, airways and digestive tract may join together to form the frontier 'commonwealth union' in order to fight the allergen. The epithelial cells are the 'engine' as well as the main target which initiates both primary and atopic inflammatory reactions. The atopic lesion may 'duplicate' the primary contacted site of cellular and molecular events. The atopic march may be due to the intrinsic 'social' involvements of the positioned epithelial cells, but may not be totally controlled by the anatomic connection or the circulating systemic factors involved in allergy pathogenesis.
皮肤、结膜、气道和消化道构成了一个巨大的易受伤害的生物表面，暴露于外部环境中。过敏原通常可以在多个部位引发过敏反应，或者导致特应性进展。然而，特应性进展的机制尚不清楚。由于目前的知识是直接针对有害因素建立的，因此人们对原发性部位和特应性部位之间的联系关注较少。过敏超敏反应表现在远离过敏原的人体部位。越来越多的证据表明，上皮细胞通过产生大量细胞因子、趋化因子和生长因子，充当引发过敏反应的“引擎”。由于上皮细胞覆盖皮肤、结膜、气道和消化道的整个表面，并且位于神经元和血液供应的末端，因此目前的解剖学和神经内分泌免疫网络知识无法轻易理解原发性部位和特应性部位之间的联系。这些巨大的易受伤害的生物表面之间有什么联系？本文重点介绍了特应性进展过敏研究的一些前沿领域，重点关注了最近在过敏进展中对原发性和特应性病变的细胞和分子事件的深入了解。特别关注巨大易受伤害表面上细胞和分子事件的同质性。基于目前可用的数据，我们得出结论，皮肤、结膜、气道和消化道可能会联合起来形成对抗过敏原的前沿“联邦联盟”。上皮细胞既是引发原发性和特应性炎症反应的“引擎”，也是主要靶标。特应性病变可能“复制”原发性接触部位的细胞和分子事件。特应性进展可能是由于定位上皮细胞的内在“社交”参与，而不是完全由过敏发病机制中涉及的解剖连接或循环系统因素控制。
