title: Effects of diesel exhaust on lung inflammation related to bacterial endotoxin in mice.
abstract: We have previously shown that intratracheal instillation of diesel exhaust particles enhances lung inflammation and lung expression of proinflammatory cytokines and chemokines related to bacterial endotoxin (lipopolysaccharide) in mice. The present study was designed to elucidate the effects of inhalation of diesel exhaust on lung inflammation related to lipopolysaccharide. ICR mice were exposed for 12 hr to clean air or diesel exhaust at a soot concentration of 0.3, 1.0, or 3.0 mg/m(3) after intratracheal challenge with 125 microg/kg of lipopolysaccharide. Lung inflammation and lung expression of proinflammatory chemokines such as macrophage chemoattractant protein-1 and keratinocyte chemoattractant were evaluated 24 hr after intratracheal administration. Diesel exhaust inhalation decreased lipopolysaccharide-elicited inflammatory cell recruitment into the bronchoalveolar lavage fluid as compared with clean air inhalation. Histological study demonstrated that exposure to diesel exhaust did not affect lipopolysaccharide-enhanced neutrophil recruitment into the lung parenchyma. Lipopolysaccharide instillation elevated lung expression of macrophage chemoattractant protein-1 and keratinocyte chemoattractant under clean air or diesel exhaust inhalation. However, diesel exhaust exposure did not influence but rather did suppress these levels in the presence of lipopolysaccharide. These results suggest that short-term exposure to diesel exhaust did not exacerbate lung inflammation related to bacterial endotoxin.
authors.affiliation: Environmental Health Sciences Division, National Institute for Environmental Studies, Ibaraki, Japan. inoue.kenichirou@nies.go.jp
authors.forename: Ken-Ichiro
authors.initials: K
authors.lastname: Inoue
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.forename: Rie
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: Miho
authors.initials: M
authors.lastname: Sakurai
authors.forename: Naoko
authors.initials: N
authors.lastname: Ueki
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Yoshikawa
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid; D002630:Chemotactic Factors / Q000235:genetics / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004359:Drug Therapy, Combination; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D007442:Intubation, Intratracheal; D008070:Lipopolysaccharides / Q000633:toxicity*; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008264:Macrophages; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D020556:Neutrophil Infiltration / Q000187:drug effects; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology; D011014:Pneumonia / Q000139:chemically induced* / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D000393:Air Pollutants; D002630:Chemotactic Factors; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D001335:Vehicle Emissions