title: Effects of diesel exhaust particles on cytokine production by splenocytes stimulated with lipopolysaccharide.
abstract: It was previously shown that pulmonary exposure of mice to diesel exhaust particles (DEP) enhances inflammatory conditions induced by allergens or bacterial endotoxin (lipopolysaccharide: LPS) via enhanced local expression of cytokines. However, resolution of the underlying mechanisms, in which DEP exaggerate inflammation, remains uncompleted. Investigation of the actions of DEP on mouse-derived mononuclear cells may provide a clue to the mechanisms, because mononuclear cells produce and release several types of cytokines. The present study elucidated the effects of DEP on mononuclear cell reactions stimulated with LPS in vitro. ICR mouse-derived mononuclear cells, isolated from splenocytes, one of the secondary lymphoid tissues, were co-cultured with LPS (1 microg ml(-1)) and DEP (1, 10 or 100 microg ml(-1)). The protein levels of interferon (IFN)-gamma, interleukin (IL)-2, IL-10, and IL-13 in the culture supernatants were measured 72 h after the co-culture. LPS significantly increased the protein levels of IFN-gamma, IL-2 and IL-10. In the presence of LPS, DEP decreased the protein levels in a concentration-dependent manner with an overall trend, whereas DEP (1, 10 microg ml(-1)) moderately elevated the IL-13 level. These results suggest that DEP suppress cytokine production from mononuclear cells stimulated with LPS and provide a possible hint for DEP facilitation on inflammatory conditions, especially related to Th2 response, in vivo.
authors.affiliation: Environmental Health Sciences Division, National Institute for Environmental Studies, Tsukuba, Japan. inoue.kenichirou@nies.go.jp
authors.forename: Ken-ichiro
authors.initials: K
authors.lastname: Inoue
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.forename: Rie
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: Miho
authors.initials: M
authors.lastname: Sakurai
authors.forename: Naoko
authors.initials: N
authors.lastname: Ueki
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Yoshikawa
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D018793:Interleukin-13 / Q000378:metabolism; D007376:Interleukin-2 / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D052638:Particulate Matter / Q000633:toxicity*; D013154:Spleen / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D018417:Th1 Cells / Q000187:drug effects / Q000378:metabolism; D018418:Th2 Cells / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D016207:Cytokines; D018793:Interleukin-13; D007376:Interleukin-2; D008070:Lipopolysaccharides; D052638:Particulate Matter; D001335:Vehicle Emissions; D016753:Interleukin-10; D007371:Interferon-gamma