DIESEL EXHAUST PARTICULATES ENHANCE EOSINOPHIL ADHESION TO NASAL EPITHELIAL-CELLS AND CAUSE DEGRANULATION

Diesel exhaust particulates (DEP) are a common air pollutant from dies el-engine-powered car exhaust and are thought to cause chronic airway diseases. On the other hand, eosinophils are major components of aller gic inflammatory disorders such as asthma, nasal allergy and atopic de rmatitis. We examined the effects of DEP and DEP extract (extract of p olyaromatic hydrocarbons) on eosinophil adhesion, survival rate and de granulation. Eosinophils, human mucosal microvascular endothelial cell s (HMMECs) and human nasal epithelial cells (HNECs) were preincubated in the presence or absence of DEP and DEP extract. S-35-labeled eosino phils were allowed to adhere to monolayers of HMMECs and HNECs. After washing, S-35 radioactivity was determined and numbers of adherent eos inophils were calculated using each standard curve. The effects of DEP and DEP extract on eosinophil survival rate and degranulation were al so determined. Although neither DEP nor DEP extract affected the adhes iveness of HMMECs and HNECs to eosinophils, 5 ng/ml of DEP extract and 50 ng/ml of DEP extract each significancy increased eosinophil adhesi veness to HNECs (134 +/- 9 and 143 +/- 8%, respectively; p < 0.01 vs. control), but neither effected eosinophil adhesiveness to HMMECs. DEP extract also induced eosinophil degranulation without changing the eos inophil survival rate. Given that eosinophil-derived lipid mediators a nd toxic proteins play important roles in the development of nasal all ergy, the above findings strongly suggest that DEP plays an important role in promoting the nasal hypersensitivity induced by enhanced eosin ophil infiltration of epithelium and eosinophil degranulation.