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血红素加氧酶-1可保护接触人造石粉尘的吸烟者,防止其肺功能测试恶化。

HO-1 protects smokers exposed to artificial stone dust for pulmonary function tests deterioration.

作者信息

Ophir Noa, Bar-Shai Amir, Kramer Mordechai R, Grubstein Ahuva, Shani Israeli Lilach, Fireman Elizabeth

机构信息

Laboratory of Pulmonary Diseases, Laboratory National Service for ILD and.

Pulmonary Department, Tel Aviv Sourasky Medical Center, Tel Aviv Israel.

出版信息

Sarcoidosis Vasc Diffuse Lung Dis. 2018;35(3):276-284. doi: 10.36141/svdld.v35i3.6968. Epub 2018 Apr 28.

DOI:10.36141/svdld.v35i3.6968
PMID:32476913
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7170158/
Abstract

The Heme Oxygenase system, along with its catabolism products, is involved in a variety of crucial physiological functions, including cytoprotection, inflammation, anti-oxidative effects, apoptosis, angiogenesis, and vascular regulation. To analyze the Heme Oxygenase -1 (HO-1) mediated effect of mild deterioration of pulmonary function testing (PFT) in exposed artificial stone smoking workers. One hundred stone workers divided into current smokers, ex-smokers and never smokers underwent Low Resolution Computed Tomography, PFT, induced sputum (IS) Particle Size Distribution (PSD) and Real Time PCR in IS samples. Smoking status had no significant effect on PFT results but it altered the IS differential cell counts. There was significantly less decline in PFT over time for the smokers group. There was a significantly lower fraction of small particles (<2 μm) in the IS of the current smokers group compared to the never- and ex-smokers groups. HO-1 gene expression was higher among smokers compared to never- and ex-smokers groups. A low percentage of small particles (<5 μm) correlated negatively to the percentage of neutrophils and positively to the percentage of macrophages in the sputum of the smokers group. We found significantly lower risk for decreased PFT deterioration among smokers workers exposed to artificial stone dust with higher HO-1 gene expression suggesting a possible protective effect of smoking by the involvement of HO-1 mechanism. .

摘要

血红素加氧酶系统及其分解代谢产物参与多种关键的生理功能,包括细胞保护、炎症、抗氧化作用、细胞凋亡、血管生成和血管调节。为了分析血红素加氧酶-1(HO-1)介导的暴露于人造石粉尘的吸烟工人肺功能测试(PFT)轻度恶化的影响。将100名石匠工人分为现吸烟者、既往吸烟者和从不吸烟者,对其进行低分辨率计算机断层扫描、PFT、诱导痰(IS)粒度分布(PSD)以及IS样本的实时聚合酶链反应。吸烟状况对PFT结果无显著影响,但会改变IS中的细胞分类计数。吸烟者组的PFT随时间的下降明显较少。与从不吸烟组和既往吸烟组相比,现吸烟者组的IS中小于2μm的小颗粒比例显著更低。与从不吸烟组和既往吸烟组相比,吸烟者中的HO-1基因表达更高。吸烟者组痰液中小于5μm的小颗粒百分比与中性粒细胞百分比呈负相关,与巨噬细胞百分比呈正相关。我们发现,HO-1基因表达较高的暴露于人造石粉尘的吸烟工人中,PFT恶化降低的风险显著更低,这表明HO-1机制参与其中,吸烟可能具有保护作用。

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ERJ Open Res. 2016 Mar 17;2(1). doi: 10.1183/23120541.00086-2015. eCollection 2016 Jan.
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Aeroparticles, Composition, and Lung Diseases.空气微粒、成分与肺部疾病。
Front Immunol. 2016 Jan 20;7:3. doi: 10.3389/fimmu.2016.00003. eCollection 2016.
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Prediction models and risk assessment for silicosis using a retrospective cohort study among workers exposed to silica in China.在中国接触二氧化硅的工人中进行回顾性队列研究,以建立矽肺病的预测模型和风险评估。
Sci Rep. 2015 Jun 19;5:11059. doi: 10.1038/srep11059.
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Outbreak of autoimmune disease in silicosis linked to artificial stone.与人造石相关的矽肺病中自身免疫性疾病的爆发。
Occup Med (Lond). 2015 Aug;65(6):444-50. doi: 10.1093/occmed/kqv073. Epub 2015 Jun 12.
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Silicosis Appears Inevitable Among Former Denim Sandblasters: A 4-Year Follow-up Study.前牛仔喷砂机工人矽肺似乎不可避免:一项4年随访研究
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