The mechanisms by which diesel exhaust particles act as an adjuvant are unknown. We hypothesized that these would be mediated through monocyte interactions with DEP.We sought to identify pathways with a role in inflammation or other signaling mechanisms that might demonstrate the mechanism of response to DEP.

Cultured human monocytes from healthy donors were cultured in the presence or absence of diesel exhaust particles. RNA was extracted following culture to determine changes in gene expression pathways.

Viera-Hutchins L, McGhee SA, Garcia-Lloret M, Chatila ZK, Girion SA, Caja R,Wise P, Ning Z, Sioutas C, Chatila TA