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反复吸入单壁碳纳米管可加重气道过敏性炎症:氧化应激的可能作用。

Repeated pulmonary exposure to single-walled carbon nanotubes exacerbates allergic inflammation of the airway: Possible role of oxidative stress.

机构信息

National Institute for Environmental Studies, Tsukuba, Ibaraki, Japan.

出版信息

Free Radic Biol Med. 2010 Apr 1;48(7):924-34. doi: 10.1016/j.freeradbiomed.2010.01.013. Epub 2010 Jan 20.

Abstract

The development of nanotechnology has increased the risk of environmental exposure to types of particles other than those derived from combustion, namely, industrial nanomaterials. Patients with bronchial asthma are sensitive to inhaled substances, including particulate matter. This study examined the effects of pulmonary exposure to a type of nano-sized carbon nanotube (single-walled nanotubes (SWCNT)) on allergic airway inflammation and sought their cellular mechanisms. In the in vivo experiments, ICR mice were divided into four experimental groups that were repeatedly administered vehicle, SWCNT (50 microg/animal), ovalbumin (OVA; an allergen), or OVA + SWCNT through an intratracheal route and thereafter assayed. SWCNT aggravated allergen-induced pulmonary inflammation with mucus hyperplasia. SWCNT with allergen amplified lung protein levels of T helper (Th) cytokines and chemokines related to allergy and exhibited adjuvant activity for allergen-specific IgG(1) (and IgE) compared with allergen alone. SWCNT accentuated the level/activity of oxidative stress-related biomarkers in the airways in the presence of allergen. In vitro, SWCNT can partially promote/strengthen the maturation/activation/function of bone marrow-derived dendritic cells (DC). Together, these results suggest that SWCNT can exacerbate murine allergic airway inflammation via enhanced activation of Th immunity and increased oxidative stress. In addition, this exacerbation may be partly through the inappropriate activation of antigen-presenting cells, including DC.

摘要

纳米技术的发展增加了环境中暴露于不同于燃烧来源的颗粒类型的风险,即工业纳米材料。支气管哮喘患者对吸入物质敏感,包括颗粒物。本研究探讨了肺部暴露于一种纳米尺寸的碳纳米管(单壁纳米管(SWCNT))对过敏性气道炎症的影响,并寻求其细胞机制。在体内实验中,将 ICR 小鼠分为四组实验组,通过气管内途径反复给予载体、SWCNT(50μg/动物)、卵清蛋白(OVA;过敏原)或 OVA+SWCNT,然后进行检测。SWCNT 加重了变应原诱导的肺部炎症和粘液增生。与仅变应原相比,SWCNT 与变应原共同放大了与过敏相关的肺 Th 细胞因子和趋化因子的蛋白水平,并表现出变应原特异性 IgG(1)(和 IgE)的佐剂活性。在存在变应原的情况下,SWCNT 加剧了气道中与氧化应激相关的生物标志物的水平/活性。在体外,SWCNT 可以部分促进/增强骨髓来源树突状细胞(DC)的成熟/激活/功能。总之,这些结果表明,SWCNT 可以通过增强 Th 免疫的激活和增加氧化应激来加重小鼠过敏性气道炎症。此外,这种加重可能部分是通过抗原呈递细胞(包括 DC)的不当激活。

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