title: Gene expression analysis of murine lungs following pulmonary exposure to Asian sand dust particles.
abstract: The respiratory health impact of Asian sand dust events originating in the deserts of China has become a concern within China and in its neighboring countries. We examined the effects of Asian sand dust particles (ASDPs) on gene expression in the murine lung using microarray analysis and elucidated the components responsible for lung inflammation. Male ICR mice were intratracheally administrated ASDPs, heat-treated ASDPs (ASDP-F, lipopolysaccaride [LPS], or beta-glucan free), or kaolin particles. We performed microarray analysis for murine lungs, the results of which were confirmed by quantitative reverse transcription-polymerase chain reaction (RT-PCR). We also assessed the protein expression and histologic changes. Exposure to ASDP, ASDP-F, or kaolin upregulated (>2-fold) 112, 36, or 9 genes, respectively, compared with vehicle exposure. In particular, ASDP exposure markedly enhanced inflammatory response-related genes, including chemokine (C-X-C motif) ligand 1/keratinocyte-derived chemokine, chemokine (C-X-C motif) ligand 2/macrophage inflammatory protein-2, chemokine (C-C motif) ligand 3/macrophage inflammatory protein-1alpha, and chemokine (C-X-C motif) ligand 10/interferon-gamma-inducible protein-10 (>6-fold). The results were correlated with those of the quantitative RT-PCR and the protein expression analyses in overall trend. In contrast, exposure to ASDP-F attenuated the enhanced expression of these proinflammatory molecules. Kaolin exposure increased the expression of genes and proteins for the chemokines. In histopathologic changes, exposure to ASDP prominently enhanced pulmonary neutrophilic inflammation, followed by kaolin and ASDP-F exposure in the order. Taken together, exposure to ASDP causes pulmonary inflammation via the expression of proinflammatory molecules, which can be attributed to LPS and beta-glucan absorbed in ASDPs. Furthermore, microarray analysis should be effective for identifying potentially novel genes, sensitive biomarkers, and pathways involved in the health effects of the exposure to environmental particles (e.g., ASDPs).
authors.affiliation: Environmental Health Sciences Division, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba 305-8506, Japan.
authors.forename: Rie
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.forename: Takamichi
authors.initials: T
authors.lastname: Ichinose
authors.forename: Katsura
authors.initials: K
authors.lastname: Mizushima
authors.forename: Masataka
authors.initials: M
authors.lastname: Nishikawa
authors.forename: Ikuko
authors.initials: I
authors.lastname: Mori
authors.forename: Ken-Ichiro
authors.initials: K
authors.lastname: Inoue
authors.forename: Kaori
authors.initials: K
authors.lastname: Sadakane
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Yoshikawa
mesh_terms: D000818:Animals; D018925:Chemokines / Q000096:biosynthesis; D002681:China; D003889:Desert Climate; D004391:Dust; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000187:drug effects*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D019570:Inhalation Exposure; D007616:Kaolin / Q000633:toxicity*; D008070:Lipopolysaccharides / Q000009:adverse effects; D008168:Lung / Q000378:metabolism* / Q000473:pathology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D020411:Oligonucleotide Array Sequence Analysis; D011014:Pneumonia / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D012822:Silicon Dioxide / Q000494:pharmacology / Q000633:toxicity*
chemical_list: D018925:Chemokines; D004391:Dust; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D007616:Kaolin; D012822:Silicon Dioxide