The late phase reaction in allergic rhinitis is now considered to be responsible for the chronic nasal obstruction in the patients with allergic rhinitis. The main pathophysiology of the late phase reaction comprises an accumulation of inflammatory ce...
The late phase reaction in allergic rhinitis is now considered to be responsible for the chronic nasal obstruction in the patients with allergic rhinitis. The main pathophysiology of the late phase reaction comprises an accumulation of inflammatory cells including eosinophils and T-lymphocytes. How these cells are preferentially recruited remains incompletely defined. Along with mast cells and other cells, they release a wide variety of mediators, cytokines, and granule constituents that can directly cause inflammation or activate local vascular endothelium to further enhance the recruitment of leukocytes through the expression and the function of adhesion molecules.
Cell adhesion molecules are now known to be critical for virtually every step in cell recruitment, including margination, transendothelial migration, chemotaxis, and transepithelial migration.
Cytokines can promote cell recruitment by altering the function and/or the expression of leukocyte, endothelial cell adhesion molecules. While the understanding of the importance of leukocytes and endothelial adhesion molecules is still at a very early stage, recent evidence has already begun to implicate these cell surface molecules in the pathogenesis of allergic diseases such as allergic rhinitis and asthma.