Response of XXXX alveolar macrophages to ultrafine, fine, and coarse urban air pollution particles.

@entity1 @entity32 @entity650 @entity5750 @entity358 @entity9536 @entity375
In the lower airways, macrophages are important regulators of @entity32 and indispensable in their antimicrobial activities. Thus, air pollution particles, which modulate airway macrophage host defenses may, in susceptible individuals, increase severity of inflammatory and infectious disease. In the present study, size fractionated, ultrafine (UF), fine (PM0.1-2.5), and coarse (PM2.5-10) particulate matter (PM) were collected from 2 urban sites in the Netherlands, and were compared for effects on @entity1 alveolar macrophages (AM). Inflammatory cytokine production, phagocytosis, and expression of phagocyte receptor @entity9536 were assessed in particle-exposed AM. @entity650 levels induced by PM2.5-10 (20411 pg/mL) were > 10-fold higher than induced by PM0.1-2.5 (1781 pg/mL). Levels induced by PM0.1-2.5 were 2- to 3-fold higher than induced by UF (770 pg/mL) when cells were exposed to the same particle mass. Cytokine induction by the PM was inhibited by antibody to @entity5750 and required the presence of serum for optimal stimulation, implying that bacterial products or endotoxin were stimulatory moieties in both coarse and fine particulate matter. Phagocytosis of opsonized @entity375 was inhibited by coarse more than by fine PM, as was @entity375 -induced oxidative burst. Coarse particles decreased @entity9536 expression more than fine PM. The UF did not affect these functions. Taken together, these results suggest that PM recognition by @entity1 AM involves receptors evolved to recognize microbial cell structures, and that microbial products preferentially found in the coarse particle fraction of PM may be involved in inflammatory events and @entity358 associated with exposure to pollution particles.
