Fine particles derived from diesel engines, diesel exhaust particles (DEP), have been shown to augment gene expression of several inflammatory cytokines in human airway epithelial cells in vitro. However, it remains unclear whether or not DEP have any effect on the expression and production of eotaxin, an important chemokine involved in eosinophil recruitment into the airways. We studied the effects of DEP by using a conventional suspended DEP and by a recently established in vitro cell exposure system to diesel exhausts (DE) ( Abe S. et al. AJRCMB 22:296-303, 2000.). DEP showed a dose-dependent stimulatory effect on eotaxin production by normal human peripheral airway epithelial cells as well as a bronchial epithelial cell line BET-1A as assessed by specific ELISA. Increased mRNA levels by DEP were shown by Northern blot analysis and reverse transcription-polymerase chain reaction (RT-PCR). DEP showed an additive effect on IL-13-stimulated eotaxin expression. DEP induced NF B activation by electrophoretic mobility shift assay as previously reported, but did not induce signal transducers and activators of transcription (STAT) 6 activation by Western blot analysis. Finally, antioxidant agents (NAC and PDTC), which inhibited NF B activation, but failed to affect STAT6 activation, almost completely attenuated DEP-induced eotaxin production, while these agents failed to attenuate IL-13-induced eotaxin production. These findings suggested that DEP stimulated eotaxin gene expression via NF B-dependent, but STAT6-independent pathways.