Airborne carbon particles (CP) are a major environmental pollutants. It is generally believed that macrophages are activated upon phagocytosis of CP. Exposure of RAW 264.7 macrophages (2 μg/ml) to PAH (polyaromatic hydrocarbon)-coated CP increases the steady state levels of TNF-α mRNA by Northern blot analysis in a time dependent manner, with initial increase of TNF-α mRNA by 1 h, peak by 8 h prior to decreasing to control levels by 24 h. The increased TNF-α mRNA levels correlated with increased TNF-α protein synthesis and secretion by Western Blot analysis and ELISA assays. PAH-CP also activated the MAPK pathway as determined by immunoprecipitation of cell lysates with ERK1/ERK2 antibody. To determine whether the MAPK pathway is involved in mediating PAH-CP-induced TNF-α expression, we pretreated the RAW cells with 10 μM PD 098059 (an inhibitor of MAPK/extracellular signal-regulated kinase-1) prior to exposure to PAH-CP. PD 098059 completely inhibited PAH-CP-induced TNF-α expression. Taken together, our study demonstrate that PAH-CP induces the inflammatory cytokine TNF-α, and that the MAPK pathway may mediate this induction.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology