Dizel egzoz partiküllerinin insan nazal epitelhücrelerinin inflamatuar parametrelerine etkisi

Although epidemiological studies have demonstrated an association between particulate air pollution and an increase in the prevalence of allergic respiratory diseases, the underlying mechanisms are not fully understood. In the present study, we aimed to investigate the effects of diesel exhaust particles (DEP) on the release of interleukin (IL)-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), regulated on activation, normal T-cell expressed and secreted (RANTES) and soluble intercellular adhesion molecule-1 (sICAM-1) from primary nasal epithelial cell (NEC) cultures from non-atopic non-rhinitic subjects (control), patients with allergic rhinitis and nasal polyposis using an explant cell culture technique. Primary NEC cultures have been incubated with 0-100 µg/ml DEP for 24 hours, and IL-8, GM-CSF, RANTES and sICAM-1 were measured by ELISA kits in the culture supernatants. Although the release of IL-8, GM-CSF and RANTES was measured in the culture supernatant, sICAM-1 was not detected. NEC cultures obtained from atopic and non-atopic polyp tissues released higher amounts of IL-8, GM-CSF and RANTES as compared to cells of control subject. Additionally, the levels of both IL-8 and RANTES was significantly gretaer in NEC cultures of atopic polyps comparing to cultures of non-atopic polyps. DEP, at concentrations of 10-100 µg/ml, did not effect the release of IL-8, GM-CSF and RANTES from NEC cultures obtained from allergic rhinitics and nasal polyps, however, only 100 µg/ml DEP significantly decreased the release of IL-8 from NECs of controls. Our results suggest that NEC cultures obtained from nasal polyps have the potential to release higher levels of inflammatory mediators, and that this is more prominent in atopic polyps. Furthermore, NEC from subjects with various pathologies may respond differently to DEP.