Comparison of inflammatory cytokine release from nasal epithelial cells of non-atopic non-rhinitic, allergic rhinitic and polyp subjects and effects of diesel exhaust particles in vitro.

BACKGROUND: Although studies have reported an association between air pollutants and increased allergic airway diseases, such as allergic rhinitis and nasal polyposis, the underlying mechanisms are not fully understood. A limited number of studies have suggested that diesel exhaust particles (DEP) play a role in atopy and the pathogenesis of allergic upper airway diseases. The aim of this study was to investigate the effect of DEP on inflammatory cytokine release, and mRNA expression of transcription factors such as JNK and NF-β in primary nasal epithelial cells (NECs), in vitro.

METHODS: NECs from non-atopic, non-rhinitic subjects (controls) and patients with allergic rhinitis and nasal polyps were cultured and incubated with 0-100μg/ml DEP for 24h. ELISA and RT-PCR were used to assess the release of IL-8, GM-CSF, and RANTES, and mRNA expression for JNK and NF-κB, respectively.

RESULTS: Compared to control cells, NECs from subjects with atopic polyps released significantly greater amounts of IL-8 (median=887 vs. 176.6pg/μg cellular protein; p<0.0001) and RANTES (median=0.191 vs. 0.02pg/μg cellular protein; p<0.001). While 50μg/ml DEP induced release of RANTES in NECs from patients with allergic rhinitis, 100μg/ml DEP decreased IL-8 levels in NECs from both control and allergic rhinitic subjects. DEP did not affect mRNA expression for JNK and NF-κB from NECs of subjects with polyps.

CONCLUSIONS: NECs from subjects with various pathologies may respond differently to DEP.