Expression of C-reactive protein and heat-shock protein-70 in the lung epithelial cell line A549, in response to PM10 exposure

Increased levels of C-reactive protein (CRP) and heat-shock protein-70 (Hsp70) in plasma are known to be associated with an increased risk of cardiovascular disease. In this study we have investigated the effects of environmental air pollution particles (PM10) and ultrafine carbon black (ufCB) on the expression of CRP and Hsp70 in the lung epithelial cell line, A549. After treatment with PM10 or ufCB the cells were found to have increased expression of CRP and Hsp70 localized in both the cell cytoplasm and nucleus. Analysis of the cell supernatants revealed that CRP and Hsp70 were present, suggesting secretion of both proteins in response to the particulate treatment. To investigate if the expression of CRP and Hsp70 was the result of free radical production, cells were treated with ufCB in the presence of antioxidants (NAL and Trolox). This revealed that antioxidants reduced the amount of CRP and Hsp70 secreted from the cells. These findings suggest that CRP and Hsp70 may be secreted from the lung epithelium as a result of oxidative stress and have important effects on the inflammatory response associated with inhalation of particulate matter.