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.