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香烟烟雾提取物可刺激人呼吸道上皮细胞产生白细胞介素-8,并可被体外超氧化物歧化酶减弱。

Cigarette smoke extract stimulates interleukin-8 production in human airway epithelium and is attenuated by superoxide dismutase in vitro.

机构信息

Department of Otolaryngology-Head and Neck Surgery, Medical University of South Carolina, Charleston, South Carolina 29425, USA.

出版信息

Am J Rhinol Allergy. 2009 Nov-Dec;23(6):e1-4. doi: 10.2500/ajra.2009.23.3400. Epub 2009 Sep 18.

DOI:10.2500/ajra.2009.23.3400
PMID:19769800
Abstract

BACKGROUND

Cigarette smoke exposure (CSE) results in extensive inflammation in the upper and lower airways. Reactive oxygen species, such as superoxide, have been shown to be potent mediators of this inflammation.

METHODS

Mucosal biopsy specimens were collected from patients undergoing sinonasal surgery and were used as a source of primary epithelial cells. Human sinonasal epithelial (HSNE) cells and were isolated from sinus tissue, maintained in culture, and ultimately treated with varying concentrations of CSE with or without free superoxide dismutase (SOD). Supernatants and cell lysates were examined for the proinflammatory cytokine interleukin (IL)-8. Similar experiments were performed using normal human bronchial epithelial (NHBE) cell lines.

RESULTS

CSE induces both secretion and intracellular production of the proinflammatory cytokine IL-8 by HSNE cells in a dose-dependent manner. Furthermore, this up-regulation can be suppressed by SOD. CSE induces secretion of IL-8 in NHBEs that is also suppressed by SOD.

CONCLUSION

Inflammation in the airway after CSE can be blocked by SOD in this in vitro model. The ability to attenuate CSE-induced inflammation with SOD could provide a therapeutic/preventative approach for individuals with cigarette smoke exposure.

摘要

背景

香烟烟雾暴露(CSE)会导致上呼吸道和下呼吸道的广泛炎症。研究表明,活性氧,如超氧自由基,是这种炎症的有效介质。

方法

从接受鼻窦手术的患者中采集黏膜活检标本,并将其用作原发性上皮细胞的来源。从鼻窦组织中分离出人鼻上皮(HSNE)细胞,在培养中维持,并最终用不同浓度的 CSE 处理,或用或不用游离超氧化物歧化酶(SOD)处理。检查上清液和细胞裂解物中促炎细胞因子白细胞介素(IL)-8 的含量。使用正常的人支气管上皮(NHBE)细胞系进行类似的实验。

结果

CSE 以剂量依赖性方式诱导 HSNE 细胞分泌和细胞内产生促炎细胞因子 IL-8。此外,这种上调可以被 SOD 抑制。CSE 诱导 NHBE 分泌 IL-8,SOD 也可以抑制这种分泌。

结论

在这个体外模型中,SOD 可以阻断 CSE 后气道中的炎症。用 SOD 减轻 CSE 诱导的炎症的能力可为暴露于香烟烟雾的个体提供一种治疗/预防方法。

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