Role of L-selectin and ICAM-1 adhesion molecules in children with asthma

Abstract

Аsthma is among the commonest chronic bronchopulmonary diseases in childhood, being a  serious medical, social and economic problem. Asthma represents a multifactorial chronic inflammatory disease characterized by activation of T-mediated factors, including adhesion molecules in bronchial mucosa, as well as minimal persistent inflammation which is characterized by a long-term inflammatory process (despite complete absence of clinical manifestations) in the patients with allergic disorders accompanied by increased expression of ICAM-1 (type 1 intercellular adhesion molecule) and CD62L (L-selectin) in the bloodstream.Lymphocyte and eosinophil counts in allergic inflammation show direct dependence on ICAM-1 contents, an intercellular adhesion molecule that provides transmigration of eosinophils and leukocytes through the endothelial barrier. Increased amount of ICAM-1 directly depends on excessive production of various reactive oxygen species in bronchial asthma. In turn, ICAM-1 induces changes in the cellular cytoskeleton which play a significant role in pathogenesis of asthma. It has been noted that ICAM-1 and CD62L molecules are those factors that exert changes at the microrheological level, including respiratory pathology of allergic nature. Increased amounts of vascular adhesion molecules in respiratory tract It has been proven are proven to be an important component of pathogenesis in bronchial asthma.Maximal expression of vascular cell adhesion molecule 1 (VCAM-1) and ICAM-1 in the persons prone to allergic diseases may occur after undetermined time period, and it immediately causes pronounced degranulation of eosinophils in respiratory tract and capillary bed. Viral infection is also an important trigger for the asthma  exacerbation. Epithelial expression of intercellular adhesion molecule ICAM-1, a cellular receptor for the most rhinoviruses, is increased after the rhinovirus infection itself. Both eosinophils and neutrophils contribute to the development of severe asthma, or exacerbation of asthma. ICAM-1 is a cellular receptor for rhinoviruses. Adhesion of eosinophils to ICAM-1 promotes functional activation of eosinophils. Therefore, adhesion of eosinophils to epithelial cells via ICAM-1 may activate this population during exacerbation in bronchial asthma.Changes in the immunohemorheology system in children with bronchial asthma represent the starting point of disorders at either hemostatic pathways, with a trend for increased adhesiveness and hypercoagulability, thus activating entire cascade of immunometabolic disorders and initiate clinical development of asthma. Exacerbation of asthma is characterized by the distinct expression pattern of the ICAM-1 adhesion factor, depending on the agent which promotes the airway obstruction. In the patients with asthma, depending on severity of exacerbation, there are pronounced changes in the levels of adhesion molecules. A pronounced increase in ICAM-1 at the time of bronchial obstruction is caused by the both causal allergen and infectious agent. However, more pronounced increase occurs during pollination, as well as slight elevation is observed in the course of obstruction caused by an infectious agent.