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Effects of diesel exhaust particles on cytokine production by splenocytes stimulated with lipopolysaccharide
Author(s) -
Inoue Kenichiro,
Takano Hirohisa,
Yanagisawa Rie,
Sakurai Miho,
Ueki Naoko,
Yoshikawa Toshikazu
Publication year - 2006
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.1187
Subject(s) - lipopolysaccharide , peripheral blood mononuclear cell , cytokine , chemistry , splenocyte , in vivo , interleukin 10 , in vitro , immunology , microbiology and biotechnology , biology , biochemistry
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 μg ml −1 ) and DEP (1, 10 or 100 μg ml −1 ). The protein levels of interferon (IFN)‐ γ , 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‐ γ , 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 μg 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 . Copyright © 2006 John Wiley & Sons, Ltd.