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Research Article

In vivo immune activation of splenocytes following exposure to tar from Asian sand dust

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Pages 649-658 | Published online: 20 Aug 2020
 

ABSTRACT

Air pollution, especially that initiated by particulate matter (PM), has been implicated as a risk factor for several inflammatory diseases. Previously, it was reported that PM enhances immune responses. PM includes the tar fraction that contains polycyclic aromatic hydrocarbons (PAHs), which produce adverse health effects in exposed individuals. However, the influence of the tar fraction (as a component of PM) on splenocytes is not fully understood. The aim of this study was to determine the effects of the tar fraction extracted from PM collected from the atmosphere in Fukuoka, Japan, on mouse splenocytes. ICR mice were administered tar (1 or 5 μg/mouse) intratracheally 4 times at 2-week intervals, and splenocytes from the tar-treated mice were extracted and examined. The parameters determined were proliferation, cytokine concentrations and transcription factors activation. Following tar treatment, splenocyte proliferation increased relative to controls. Concanavalin A (ConA)-induced interleukin (IL)-2 formation and ConA- or lipopolysaccharide (LPS)-induced interferon-γ production were elevated in splenocytes from tar-exposed mice. However, the production of tumor necrosis factor-α and IL-6 induced by LPS was not markedly changed following tar treatment. Further, nuclear factor of activated T cells, but not nuclear factor-κB, was enhanced in splenocytes of tar-exposed mice. Data indicate that tar-activated splenocytes and PM-bound PAHs might contribute to T cell activation in the spleen.

Disclosure statement

The authors declare that they have no conflict of interest.

Supplementary material

Supplemental data for this article can be accessed here

Additional information

Funding

This work was supported by a Grant-in-Aid from the Environment Research and Technology Development Fund [ERTDF 5-1457] from the Ministry of the Environment, Government of Japan, to Y. Yoshida and T. Ichinose and by a Grant-in-Aid for Scientific Research (B) [No. 24390159] from the Japan Society for the Promotion of Science to Y. Yoshida and Scientific Research (B) from the Japan Society for the Promotion of Science to T. Mimura and Y. Yoshida [grant number #20H04347].

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