Diesel exhaust particles (
DEP) induce
pulmonary diseases including
asthma and
chronic bronchitis. Comprehensive evaluation is required to know the effects of
pollutants including
DEP on these and other
lung diseases. Alveolar macrophages (AM) and epithelial cells are important cellular targets for
pollutants such as
DEP in the lung. Alveolar macrophages encounter and phagocytose
DEP in the alveolar space, and their biological responses have been implicated in
DEP-induced
pulmonary diseases. Expression profiles of genes induced by
DEP in AM will lead to better understanding of the mechanisms involved in
pulmonary diseases. To characterize the effect of the
DEP extract on AM systematically, we analyzed the gene expression in AM exposed to
DEP extract using the Atlas Rat Toxicology Array II. The finding in
cDNA microarray was further confirmed by Northern blot analysis. AM were exposed to 10 microg/ml of
DEP extract for 6 h in order to elucidate early response to
DEP extract in AM. Early response to
DEP extract in AM may affect the alteration of gene expression in subsequent responses so that it is important to identify the alteration in early response. In this study, the transcription of 6 genes in the
cDNA microarray was significantly elevated by exposure of the AM to
DEP extract. These genes were
heme oxygenase (HO)-1 and -2,
thioredoxin peroxidase 2 (TDPX-2),
glutathione S-transferase P subunit (GST-P),
NAD(P)H
dehydrogenase, and
proliferating cell nuclear antigen (
PCNA). The antioxidative
enzymes such as HO, TDPX-2, GST-P, and
NAD(P)H
dehydrogenase may play a role in the pulmonary defense against oxidative stress caused by various
pollutants including
DEP.
PCNA may have contributed to the repair of DNA damage and to cell proliferation caused by exposure to these
pollutants. Our results suggest that
cDNA microarray analysis is a useful tool to investigate the biological responses to pulmonary toxicants.