Soluble adhesion molecules and cytokines in perennial allergic rhinitis

Background: increasing evidence suggests adhesion molecules and cytokines in patients with inflammatory airway diseases are involved in steps of entrapment and migration of inflammatory cells. Recently, soluble forms of adhesion molecules and cytokines have been detected in the sera and other body fluids of patients with various diseases. Objective: Eosinophilia in nasal mucosa is characteristic of allergic rhinitis. Vascular adhesion molecules expressed on the endothelium are essential for eosinophils to move from the peripheral blood into the sites of inflammation. Herein, soluble forms of vascular adhesion molecules and eosinophil-activating cytokines are measured to investigate the significance of their appearance in the sera with eosinophil infiltration in the nasal mucosa of perennial allergic rhinitis. Methods: With the quantitative sandwich enzyme immunoassay technique, the sera of 36 patients of perennial allergic rhinitis and 20 nonatopic subjects were used to measure the levels of soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (endothelial leukocyte adhesion molecule-1, sELAM-1), interleukin-3 (IL-3), and interleukin-5 (IL-5). Results: No significant differences in the levels of soluble vascular adhesion molecules were noted between the two groups. Eosinophil-activating cytokines, IL-3 and IL-5, were significantly increased in the group with perennial allergic rhinitis, and were correlated with eosinophil infiltration in nasal scrapings. Conclusion: Although the vascular adhesion molecules expressed on the endothelium are necessary for eosinophils to appear in allergic tissues, eosinophil-activating cytokines as IL-3 and IL-5 are Likely to be essential for eosinophils to function in tissues. The elevated concentrations of IL-3 and IL-5 in allergic rhinitis may reflect the inflammatory response occurring in the T cell activation and in relation to manifestation of eosinophils.