Abstract
More than one mechanism contributes to persistent increases in eosinophils in the nasal cavity and paranasal sinus. The levels of eotaxin in lavage samples obtained after antigen challenge showed strong correlation with lavage levels of eosinophil counts and eosinophil protein-X. In the eosinophil endothelial transmigration (TEM) assay using nasal microvascular endothelial cells, eotaxin showed the most potent effect among various eosinophil chemoattractants. In addition, treatment of eosinophils with anti-CCR3 mono- clonal antibody significantly blocked eosinophil TEM induced by homogenate of nasal mucosa. These results indicate that eotaxin has an important role in eosinophil-dependent inflammation in nasal mucosa and suggest that blocking eotaxin or CCR-3 may be useful for new therapeutic tools of allergic rhinitis. Several mechanisms for eosinophilic inflammation in paranasal sinus may be proposed: a series of reaction systems may be involved, such as swollen mucosa caused by type I allergic reactions in the nasal cavity, closure of natural orifices, a hypoxic state in the maxillary sinus, accelerated production of eotaxin and RANTES from fibroblasts and eosinophilic infiltration. These reaction systems would include tumor necrosis factor-α and interferon-γ, as well as Th2 cytokines, including interleukin-4 and -13, so that this phenomenon hardly occurs in infective rhinitis.
