The present study was performed to further improve our understanding of the molecular mechanisms involved in the activation of NFκB, a major transcriptional factor involved in the inflammatory response in the inflammatory response in the lung, by particulate matter in lung epithelial cells wit an aerodynamic diameter of less than 2.5 micro meter(PM2.5).

Immediate production of reactive oxygen species (ROS) and nitrogen species (RNS), with the PM2.5 induced expression of inducible nitric oxide synthase (iNOS), IkB degradatio and NFκB-dependent transcrptional activity, in A 549 cells, were monitored. Addition, we also examined the effect of the iNOS inhibitor, L-N6-(1-iminoethyl) lysine hydrochloride (L-NIL), on the PM 2.5-induced NFκB activation in A 549 cells.

The rapid degradation of IkB and the increase of transcriptional activity of the NFκB-dependent promotor were observed in A 549 cells exposed to PM2.5. The immediate production of ROS in response to PM2.5 in A 549 cells was not clearly detected, although immediate responses were observed in RAW 264.7 cells. A549 cells, cultured in the presence of PM2.5, produced an increase in NO, which was noticeably significant after 15 min of exposure with the expression of iNOS mRNA. The addition of L-NIL, an iNOS inhibitor, significantly inhibited the PM2.5-induced IkB degradation and the increase of the NFκB-dependent transcriptional activity.

These results suggest that PM2.5 stimulates the immediate production of RNS, leading to the activation of NFκB in the pulmonary epithelium.