4.2 Article

Effects of nanoparticle-rich diesel exhaust particles on IL-17 production in vitro

期刊

JOURNAL OF IMMUNOTOXICOLOGY
卷 9, 期 1, 页码 72-76

出版社

TAYLOR & FRANCIS LTD
DOI: 10.3109/1547691X.2011.629638

关键词

Nanoparticle; diesel exhaust particles; IL-17; ROR gamma t

资金

  1. Japan Society for the Promotion of Science [18390188]
  2. Grants-in-Aid for Scientific Research [18390188] Funding Source: KAKEN

向作者/读者索取更多资源

It has been shown that pulmonary exposure to diesel exhaust particles (DEP) disrupt immune systems, presenting as exacerbating effects on allergic manifestations (e. g., allergic asthma). To date, the impact of nano-level DEP on health has not been fully elucidated. Our institute (the National Institute for Environmental Studies) established an 'environmental nanoparticle exposure system applied in animals' in 2005 and, since then, the health effects of exposures to these types of agents have been explored. The present study was designed to investigate the in vitro effects of nanoparticle-rich DEP (NRDEP) on primary splenocytes from atopy-prone hosts. NC/Nga mouse-derived splenic mononuclear cells were co-cultured with NRDEP (0-50 mu g/ml); thereafter, cell viability/proliferation was evaluated via a WST-1 assay, production/release of interleukin (IL)-17A in the culture supernatants by ELISA, and expression of ROR gamma t (retinoic acid-related orphan receptor-gamma t) in cell lysates by Western blot analyses. The results indicated that NRDEP reduced cell viability/proliferation in a dose-related manner-significantly so at a level of 50 mu g/ml NRDEP. In contrast, up to 10 mu g NRDEP/ml increased ROR gamma t expression in the splenocytes and subsequent IL-17A production/release by the cells in a dose-dependent manner with an overall trend (with significance vs 1 mu g NRDEP/ml and 10 mu g NRDEP/ml for IL-17A); 50 mu g NRDEP/ml tended to inhibit the transcription factor expression and cytokine production/release. These results suggest that NRDEP can activate naive splenic mononuclear cells from atopy-prone animals in terms of ROR gamma t and IL-17A induction (T(H)17 response).

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