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电子烟蒸汽增强肺炎链球菌对气道上皮细胞的黏附。

E-cigarette vapour enhances pneumococcal adherence to airway epithelial cells.

机构信息

Centre for Genomics and Child Health, Blizard Institute, Queen Mary University of London, London, UK.

The Dept of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, UK.

出版信息

Eur Respir J. 2018 Feb 7;51(2). doi: 10.1183/13993003.01592-2017. Print 2018 Feb.

DOI:10.1183/13993003.01592-2017
PMID:29437942
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7614837/
Abstract

E-cigarette vapour contains free radicals with the potential to induce oxidative stress. Since oxidative stress in airway cells increases platelet-activating factor receptor (PAFR) expression, and PAFR is co-opted by pneumococci to adhere to host cells, we hypothesised that E-cigarette vapour increases pneumococcal adhesion to airway cells.Nasal epithelial PAFR was assessed in non-vaping controls, and in adults before and after 5 min of vaping. We determined the effect of vapour on oxidative stress-induced, PAFR-dependent pneumococcal adhesion to airway epithelial cells , and on pneumococcal colonisation in the mouse nasopharynx. Elemental analysis of vapour was done by mass spectrometry, and oxidative potential of vapour assessed by antioxidant depletion There was no difference in baseline nasal epithelial PAFR expression between vapers (n=11) and controls (n=6). Vaping increased nasal PAFR expression. Nicotine-containing and nicotine-free E-cigarette vapour increased pneumococcal adhesion to airway cells Vapour-stimulated adhesion was attenuated by the PAFR blocker CV3988. Nicotine-containing E-cigarette vapour increased mouse nasal PAFR expression, and nasopharyngeal pneumococcal colonisation. Vapour contained redox-active metals, had considerable oxidative activity, and adhesion was attenuated by the antioxidant N-acetyl cysteine.This study suggests that E-cigarette vapour has the potential to increase susceptibility to pneumococcal infection.

摘要

电子烟蒸汽中含有自由基,有可能引发氧化应激。由于气道细胞中的氧化应激会增加血小板激活因子受体(PAFR)的表达,而 PAFR 被肺炎球菌利用来黏附宿主细胞,我们假设电子烟蒸汽会增加肺炎球菌对气道细胞的黏附。我们评估了非电子烟使用者和电子烟使用者在吸电子烟前和吸电子烟后 5 分钟的鼻上皮 PAFR。我们确定了蒸汽对氧化应激诱导的、依赖 PAFR 的肺炎球菌对气道上皮细胞的黏附的影响,以及对小鼠鼻咽部肺炎球菌定植的影响。通过质谱分析法对蒸汽进行元素分析,并通过抗氧化剂消耗法评估蒸汽的氧化潜能。电子烟使用者(n=11)和对照组(n=6)之间鼻上皮 PAFR 表达的基线无差异。吸电子烟会增加鼻 PAFR 表达。含尼古丁和不含尼古丁的电子烟蒸汽会增加肺炎球菌对气道细胞的黏附。PAFR 阻滞剂 CV3988 可减弱蒸汽刺激的黏附。含尼古丁的电子烟蒸汽增加了小鼠鼻 PAFR 表达和鼻咽部肺炎球菌定植。蒸汽中含有氧化还原活性金属,具有相当大的氧化活性,而抗氧化剂 N-乙酰半胱氨酸可减弱黏附。这项研究表明,电子烟蒸汽有可能增加对肺炎球菌感染的易感性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0116/7614837/a27e7cd79924/EMS181594-f007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0116/7614837/a27e7cd79924/EMS181594-f007.jpg

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