干旱区生态环境知识资源中心(Arid): Critical role of IL-33, but not IL-25 or TSLP, in silica crystal-mediated exacerbation of allergic airway eosinophilia

Arid

DOI	10.1016/j.bbrc.2020.09.046
	Critical role of IL-33, but not IL-25 or TSLP, in silica crystal-mediated exacerbation of allergic airway eosinophilia
	Unno, Hirotoshi; Arae, Ken; Matsuda, Akira; Ikutani, Masashi; Tamari, Masato; Motomura, Kenichiro; Toyama, Sumika; Suto, Hajime; Okumura, Ko; Matsuda, Akio; Morita, Hideaki; Sudo, Katsuko; Saito, Hirohisa; Matsumoto, Kenji; Nakae, Susumu
通讯作者	Nakae, S
来源期刊	BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN	0006-291X
EISSN	1090-2104
出版年	2020
卷号	533 期号:3 页码:493-500
英文摘要	Silica crystals (silica), which are a major mineral component of volcanic ash and desert dust, contribute to the pathogenesis of pulmonary disorders such as asthma and fibrosis. Although administration of silica or sand dust to rodents exacerbates development of ovalbumin-induced or house dust mite-induced asthma-like airway inflammation, the detailed mechanisms remain unclear. Here, using murine models, we found that silica can induce IL-33 expression in pulmonary epithelial cells. IL-33, but not IL-25 or TSLP, and type 2 cytokines such as IL-5 and IL-13 were critically involved in silica's exacerbation of OVA-induced airway eosinophilia in mice. Innate lymphoid cells (ILCs), but not T, B or NKT cells, were also involved in the setting. Moreover, a scavenger receptor that recognized silica was important for silica's exacerbating effect. These observations suggest that IL-33 induced in epithelial cells by silica activates ILCs to produce IL-5 and/or IL-13, contributing to silica's exacerbation of OVA-induced airway eosinophilia in mice. Our findings provide new insight into the underlying mechanisms of exacerbation of pulmonary disorders such as asthma following inhalation of silica-containing materials such as volcanic ash and desert dust. (C) 2020 Elsevier Inc. All rights reserved.
英文关键词	Asthma Silica Interleukin-33 Scavenger receptor Innate lymphoid cells
类型	Article
语种	英语
开放获取类型	Bronze
收录类别	SCI-E
WOS记录号	WOS:000588268300035
WOS关键词	INNATE LYMPHOID-CELLS ; INFLAMMATION ; ASTHMA ; DUST ; RESPONSES ; EXPOSURE
WOS类目	Biochemistry & Molecular Biology ; Biophysics
WOS研究方向	Biochemistry & Molecular Biology ; Biophysics
资源类型	期刊论文
条目标识符	http://119.78.100.177/qdio/handle/2XILL650/327452
作者单位	[Unno, Hirotoshi; Tamari, Masato] Jikei Univ, Dept Pediat, Sch Med, Tokyo 1058461, Japan; [Unno, Hirotoshi; Arae, Ken; Tamari, Masato; Motomura, Kenichiro; Toyama, Sumika; Matsuda, Akio; Morita, Hideaki; Saito, Hirohisa; Matsumoto, Kenji] Natl Res Inst Child Hlth & Dev, Dept Allergy & Clin Immunol, Tokyo 1578535, Japan; [Arae, Ken] Kyorin Univ, Fac Hlth Sci, Dept Immunol, Tokyo 1818612, Japan; [Matsuda, Akira] Juntendo Univ Sch, Dept Ophthalmol, Lab Ocular Atop Dis, Tokyo 1138412, Japan; [Ikutani, Masashi; Nakae, Susumu] Hiroshima Univ, Grad Sch Integrated Sci Life, 1-4-4 Kagamiyama, Higashihiroshima, Hiroshima 7398528, Japan; [Suto, Hajime; Okumura, Ko] Juntendo Univ, Atopy Res Ctr, Grad Sch Med, Tokyo 1138412, Japan; [Sudo, Katsuko] Tokyo Med Univ, Anim Res Ctr, Tokyo 1608402, Japan; [Nakae, Susumu] Univ Tokyo, Ctr Expt Med & Syst Biol, Inst Med Sci, Lab Syst Biol, Tokyo 1088639, Japan; [Nakae, Susumu] Japan Sci & Technol Agcy, Precursory Res Embryon Sci & Technol, Saitama 3320012, Japan
推荐引用方式 GB/T 7714	Unno, Hirotoshi,Arae, Ken,Matsuda, Akira,et al. Critical role of IL-33, but not IL-25 or TSLP, in silica crystal-mediated exacerbation of allergic airway eosinophilia[J],2020,533(3):493-500.
APA	Unno, Hirotoshi.,Arae, Ken.,Matsuda, Akira.,Ikutani, Masashi.,Tamari, Masato.,...&Nakae, Susumu.(2020).Critical role of IL-33, but not IL-25 or TSLP, in silica crystal-mediated exacerbation of allergic airway eosinophilia.BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,533(3),493-500.
MLA	Unno, Hirotoshi,et al."Critical role of IL-33, but not IL-25 or TSLP, in silica crystal-mediated exacerbation of allergic airway eosinophilia".BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 533.3(2020):493-500.