Vascular endothelial cells and eosinophil infiltration in allergic rhinitis

Abstract

SummaryEosinophils, as well as mast cells, play an important role in inducing the clinical symptoms of allergic rhinitis (AR), especially in the late‐phase response. Adhesion molecules, type 2 helper T (Th2) cell cytokines, CC chemokines, and eicosanoids from mast cells are key players of the pathophysiological mechanism of eosinophil transendothelial migration and accumulation in nasal mucosa. While tethering and adhesion of eosinophils to nasal microvascular endothelial cells are the critical steps, and adhesion molecules and their ligands expressed on eosinophils and endothelial cells have been well studied, regulation of these adhesion molecules and ligands by Th2 cytokines and CC chemokines is thought to be a very important mechanism of eosinophil migration. Eicosanoids such as cysteinyl leucotrienes (CysLTs) and thromboxanes (TXs) from mast cells are also considered to be major factors effective in the expression of adhesion molecules and their ligands, and eicosanoid receptors are thought to be distributed on nasal mucosal endothelial cells. For transendothelial migration, increasing vascular permeability is an indispensable step after trapping eosinophils in nasal microvasculature. While histamine is one of the best known vasodilators in AR, especially in the acute‐phase reaction, CysLTs and vascular endothelial growth factor (VEGF) are also effective vasodilators. Much of the evidence to date has been obtained using commercial cell lines of human umbilical vein endothelial cells (HUVEC), which may have cellular characteristics different from human nasal mucosal endothelial cells. Further studies of human nasal mucosa seem necessary to investigate the mechanisms of eosinophil recruitment in nasal mucosa of AR.