کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2602304 | 1133391 | 2007 | 10 صفحه PDF | دانلود رایگان |

Exposure to ambient particulate matter (PM) is responsible for airway inflammation and tissue remodeling. Urban PM2.5 (aerodynamic diameter <2.5 μm) is a complex mixture rich in soots and containing hydrosoluble and organic components. We previously showed that the exposure of airway epithelial cells to PM2.5 triggers the release of amphiregulin (AR), ligand of the epidermal growth factor receptor (EGFR) involved in proinflammatory and repair responses.The effect of Paris PM2.5 organic and aqueous fractions in AR expression and secretion was investigated on the bronchial epithelial cell line 16HBE and normal human nasal epithelial (NHNE) cells. Both a macroarray specific for inflammation pathways and RT-PCR showed an AR upregulation in organic extract-treated 16HBE cells. AR release is induced in 16HBE and NHNE cells grown on plastic and exposed to native PM2.5, organic extract and to a lesser extent washed PM2.5 (deprived of its hydrosoluble content) and aqueous extract. Furthermore, as assessed by using NHNE cells grown on Transwell inserts, this secretion is polarized toward the basolateral side where the EGFR is expressed.To conclude, both PM2.5 organic and hydrosoluble components are involved in the expression and secretion of AR; organic compounds exhibiting a strong effect when they are easily bioavailable.
Journal: Toxicology Letters - Volume 168, Issue 2, 30 January 2007, Pages 155–164