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

Abstract

Abstract. 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.

Research Progress in Atopic March

“…This may be a systemic reaction of the body, and the mechanisms are incompletely understood. Through literature search, Luo et al proposed a model of “social events” of cells and molecules to explain the atopic march ( 90 ). Epithelial cells, such as epidermal keratinocytes and airway epithelial cells, are the first line of defense against allergen exposure and initiate the inflammatory response by releasing proinflammatory cytokines.…”

Cannabinoids and Inflammations of the Gut-Lung-Skin Barrier

“…The epithelial cells produce thymic stromal lymphopoietin (TSLP), a cytokine similar to IL-7, which is involved in the allergic response and is a key factor in the onset of allergic inflammation in the skin, lungs and gastrointestinal tract [15]. TSLP is considered to be a biomarker for disruptions of the epithelial integrity, and was cited as a determining and aggravating factor in a variety of allergy models, including ovalbumin (OVA)-induced asthma, atopic dermatitis and allergic diarrhea [16].…”

Original Research: Extract ofBambusae Caulis in Taeniaminhibits cigarette smoke-induced pulmonary and intestinal inflammation

“…It is supported by numerous studies that organs sharing common embryological origins may communicate with each other even if there is no anatomical association. [27][28][29][30][31][32][33][34][35][36] The primitive foregut has been shown from a growing number of literatures as the embryological origin of respiratory and gastrointestinal epithelia. 37,38 Wang et al 39 indicated the existence of the lung-intestine communication by presenting the lung's duplication of inflammatory reactions in the bowel.…”