The mechanism of atopic march may be the ‘social’ event of cells and molecules (Review)

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.