Am. J. Respir. Cell Mol. Biol., Volume 19, Number 4, October, 1998 672-680

Induction of the Lung Myofibroblast PDGF Receptor System by Urban Ambient Particles from Mexico City

James C. Bonner, Annette B. Rice, Pamela M. Lindroos, Patricia O. O'Brien, Kevin L. Dreher, Irma Rosas, Ernesto Alfaro-Moreno, and Alvaro R. Osornio-Vargas

Airway Inflammation Section, Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park; National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina; Division of Basic Investigation, National Cancer Institute, Mexico City; and Centers of Study for the Atmosphere, UNAM, Mexico City, Mexico

Platelet-derived growth factor (PDGF) and its receptor system regulate mesenchymal cell proliferation. We recently reported that emission-source fly-ash particles and asbestos fibers induce the PDGF -receptor through a macrophage-dependent pathway, and upregulation of this receptor greatly enhances the mitogenic response of lung myofibroblasts to PDGF (Lindroos and colleagues, Am. J. Respir. Cell Mol. Biol. 1997;16:283-292). In the present study we investigated the effect of particulate matter  10 µm in size (PM₁₀) from the southern, central, and northern regions of Mexico City on PDGF receptor induction and compared these urban, ambient particles with Mt. St. Helen's volcanic ash particles as a negative control. All Mexico City PM₁₀ samples, but not volcanic ash, stimulated rat alveolar macrophages to secrete a soluble, upregulatory factor(s) for the PDGF -receptor on early passage rat lung myofibroblasts. The macrophage-derived upregulatory activity was blocked by the interleukin (IL)-1 receptor antagonist. The ability of PM₁₀ to stimulate IL-1 release was blocked in part by a recombinant endotoxin neutralizing protein (rENP). Lipopolysaccharide/endotoxin (LPS) and vanadium, both constituents that were present within these PM₁₀ samples, also stimulated macrophages to secrete factor(s) that upregulated PDGF-R on lung myofibroblasts. Direct exposure of myofibroblasts to PM₁₀ also elicited upregulation of the PDGF -receptor, and this effect was blocked by rENP and mimicked by LPS, but not vanadium. These findings suggest that PM₁₀ particles induce expression of the PDGF receptor system through macrophage-dependent and -independent mechanisms involving endotoxin and metals.

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