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Components of diesel exhaust particles differentially affect lung expression of cyclooxygenase‐2 related to bacterial endotoxin
Author(s) -
Inoue Kenichiro,
Takano Hirohisa,
Yanagisawa Rie,
Ichinose Takamichi,
Sadakane Kaori,
Yoshino Shin,
Yamaki Kouya,
Uchiyama Kazuhiko,
Yoshikawa Toshikazu
Publication year - 2004
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.984
Subject(s) - lipopolysaccharide , chemistry , cyclooxygenase , lung , pharmacology , gene expression , andrology , immunology , enzyme , biochemistry , medicine , biology , gene
We have reported previously that components of diesel exhaust particles (DEP) differently affect acute lung injury related to lipopolysaccharide (LPS) in mice. This study examined the effects of components of DEP on the lung expression of cyclooxygenase (COX)‐1 and ‐2 in the presence or absence of LPS. ICR mice were divided into six experimental groups that received vehicle, LPS (2.5 mg kg −1 ), organic chemicals in DEP (DEP‐OC) extracted with dicloromethane (4 mg kg −1 ), residual carbonaceous nuclei after the extraction (washed DEP: 4 mg kg −1 ), DEP‐OC (4 mg kg −1 ) + LPS (2.5 mg kg −1 ) or washed DEP (4 mg kg −1 ) + LPS (2.5 mg kg −1 ) intratracheally. The expression of mRNA for both COXs in the lung was evaluated 4 h after the intratracheal administration. The magnitude of COX‐1 mRNA expression was not altered in each group. The LPS treatment enhanced the COX‐2 gene expression compared with vehicle treatment. Washed DEP combined with LPS further increased its expression compared with LPS alone. In contrast, combined treatment of DEP‐OC with LPS decreased COX‐2 gene expression compared with LPS alone. These results suggest that the residual carbonaceous nuclei of DEP predominantly enhance lung expression of COX‐2 rather than the extracted organic chemicals from DEP in the presence of LPS, which is concomitant with the magnitude of acute lung injury in our previous study. Copyright © 2004 John Wiley & Sons, Ltd.