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Title: Biological factor related to Asian sand dust particles contributes to the exacerbation of asthma
Authors: Honda, Akiko  kyouindb  KAKEN_id  orcid (unconfirmed)
Sawahara, Takahiro
Hayashi, Tomohiro
Tsuji, Kenshi
Fukushima, Wataru
Oishi, Mizuki
Kitamura, Gaku
Kudo, Hitomi
Ito, Sho
Yoshida, Seiichi
Ichinose, Takamichi
Ueda, Kayo  kyouindb  KAKEN_id  orcid (unconfirmed)
Takano, Hirohisa  kyouindb  KAKEN_id
Author's alias: 本田, 晶子
上田, 佳代
高野, 裕久
Keywords: Asian sand dust particles
Bjerkandera adusta
bone‐marrow‐derived antigen presenting cells
Issue Date: May-2017
Publisher: Wiley
Journal title: Journal of Applied Toxicology
Volume: 37
Issue: 5
Start page: 583
End page: 590
Abstract: Epidemiologic studies have revealed that Asian sand dust particles (ASDs) can affect respiratory and immune health represented by asthma. Factors responsible for the exacerbation of asthma remain unclear. The fungus Bjerkandera adusta ( and polycyclic aromatic hydrocarbons such as benzo[a]pyrene (BaP) have been identified in ASDs collected from the atmosphere when an ASD event occurred. We investigated the effects of and BaP related to ASDs on respiratory and immune systems. Bone marrow‐derived antigen‐presenting cells (APCs) and splenocytes from atopic prone NC/Nga mice and human airway epithelial cells were exposed to the or to BaP in the presence and absence of heated‐ASDs (H‐ASDs). and BaP in both the presence and absence of H‐ASDs increased the expression of cell surface molecules on APCs. H‐ASDs alone slightly activated APCs. The expressions induced by were higher than those induced by BaP in the presence and absence of H‐ASDs. There were no remarkable effects on the activation of splenocytes or the proinflammatory responses in airway epithelial cells. These results suggest that rather than BaP contributes to the exacerbation of asthma regardless of the presence or absence of sand particles, particularly by the activation of the immune system via APCs.
Rights: This is the peer reviewed version of the following article: 'Journal of Applied Toxicology' 37(5) 583-590, which has been published in final form at This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.
The full-text file will be made open to the public on 27 March 2018 in accordance with publisher's 'Terms and Conditions for Self-Archiving'.
This is not the published version. Please cite only the published version.
DOI(Published Version): 10.1002/jat.3395
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