Effects of organic chemicals derived from ambient particulate matter on lung inflammation related to lipopolysaccharide.
The effects of components of ambient particulate matter (PM) on individuals with predisposing respiratory disorders are not well defined. We have previously demonstrated that airway exposure to diesel exhaust particles (DEP) or organic chemicals (OC) extracted from DEP (DEP-OC) enhances lung inflammation related to bacterial endotoxin (lipopolysaccharide, LPS). The present study aimed to examine the effects of airway exposure to OC extracted from urban PM (PM-OC) on lung inflammation related to LPS. ICR mice were divided into four experimental groups that intratracheally received vehicle, LPS (2.5 mg/kg), PM-OC (4 mg/kg), or PM-OC + LPS. Lung inflammation, lung water content, and lung expression of cytokines were evaluated 24 h after intratracheal administration. LPS challenge elicited lung inflammation evidenced by cellular profiles of bronchoalveolar lavage fluid and lung histology, which was further aggravated by the combined challenge with PM-OC. The combination with PM-OC and LPS did not significantly exaggerate LPS-elicited pulmonary edema. LPS instillation induced elevated lung expression of interleukin-1beta, macrophage inflammatory protein-1alpha, macrophage chemoattractant protein-1, and keratinocyte chemoattractant, whereas the combined challenge with PM-OC did not influence these levels. All the results were consistent with our previous reports on DEP-OC. These results suggest that the extracted organic chemicals from PM exacerbate infectious lung inflammation. The mechanisms underlying the enhancing effects are not mediated via the enhanced local expression of proinflammatory cytokines.
Inoue
Ken-ichiro
K
Environmental Health Sciences Division, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba 305-8506 Ibaraki, Japan.
Takano
Hirohisa
H
Yanagisawa
Rie
R
Hirano
Seishiro
S
Kobayashi
Takahiro
T
Ichinose
Takamichi
T
Yoshikawa
Toshikazu
T
D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D018932:Chemokine CCL2 / Q000378:metabolism; D054407:Chemokine CCL4; D018925:Chemokines / Q000378:metabolism; D004195:Disease Models, Animal; D053583:Interleukin-1beta / Q000378:metabolism; D008070:Lipopolysaccharides; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D019402:Macrophage Inflammatory Proteins / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D020556:Neutrophil Infiltration / Q000187:drug effects; D009504:Neutrophils / Q000187:drug effects / Q000473:pathology; D009930:Organic Chemicals / Q000302:isolation & purification / Q000633:toxicity*; D052638:Particulate Matter / Q000737:chemistry / Q000633:toxicity*; D011014:Pneumonia / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D011654:Pulmonary Edema / Q000139:chemically induced / Q000473:pathology
D000393:Air Pollutants; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D054407:Chemokine CCL4; D018925:Chemokines; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D019402:Macrophage Inflammatory Proteins; D009930:Organic Chemicals; D052638:Particulate Matter; C482199:lipopolysaccharide, E coli O55-B5; C074302:keratinocyte-derived chemokines