Tobacco smoke induced COPD/emphysema in the animal model-are we all on the same page?
Tobacco smoke induced COPD/emphysema in the animal model-are we all on the same page?
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DOI：
10.3389/fphys.2013.00091
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发表时间：
2013
影响因子：
4
通讯作者：
Taraseviciene-Stewart L
中科院分区：
文献类型：
--
作者：
Leberl M;Kratzer A;Taraseviciene-Stewart L
慢性阻塞性肺疾病（COPD）是全球最主要的死亡原因之一。它主要由烟草烟雾引起，使其成为一种容易预防的疾病，但由遗传性α-1抗胰蛋白酶缺乏症促进。除了主动吸烟者外，非自愿接触二手烟（SHS）的人也会出现健康问题。目前，SHS和COPD之间的关系还没有很好地建立。对致病机制的了解有限，从而阻碍了这种对社会和经济有害的疾病的新治疗方法的进展。在这里，我们试图总结在动物模型中进行的烟草烟雾研究，应用主流（直接，仅鼻子）和侧流（间接，全身）烟雾暴露。这篇综述了155项研究，比较了COPD发展的细胞和分子机制以及蛋白水解、炎症和血管反应性反应。这是一项困难的任务，因为对于大多数实验，暴露参数的列表是有限的。我们表明，主流研究和SHS研究在很大程度上都呈现出类似的以巨噬细胞为主的炎症细胞群以及升高的趋化因子/细胞因子水平，例如TNF-α。此外，SHS，像主流烟雾，已被证明会导致血管重塑和中性粒细胞弹性蛋白酶介导的蛋白水解基质分解，无法修复。在两种接触情况下，疾病机制和治疗干预似乎是一致的。抗氧化治疗是应用最广泛的干预措施之一，对主流和SHS都是成功的。本文中直接与间接烟雾暴露研究的比较强调，尽管有许多重叠的途径，但SHS在COPD发病机制中使用与直接烟雾完全相同的机制并不能得出结论，但应被视为可预防的健康风险。SHS相关COPD存在一些独特的特征和治疗选择。
Chronic Obstructive Pulmonary Disease (COPD) is one of the foremost causes of death worldwide. It is primarily caused by tobacco smoke, making it an easily preventable disease, but facilitated by genetic α-1 antitrypsin deficiency. In addition to active smokers, health problems also occur in people involuntarily exposed to second hand smoke (SHS). Currently, the relationship between SHS and COPD is not well established. Knowledge of pathogenic mechanisms is limited, thereby halting the advancement of new treatments for this socially and economically detrimental disease. Here, we attempt to summarize tobacco smoke studies undertaken in animal models, applying both mainstream (direct, nose only) and side stream (indirect, whole body) smoke exposures. This overview of 155 studies compares cellular and molecular mechanisms as well as proteolytic, inflammatory, and vasoreactive responses underlying COPD development. This is a difficult task, as listing of exposure parameters is limited for most experiments. We show that both mainstream and SHS studies largely present similar inflammatory cell populations dominated by macrophages as well as elevated chemokine/cytokine levels, such as TNF-α. Additionally, SHS, like mainstream smoke, has been shown to cause vascular remodeling and neutrophil elastase-mediated proteolytic matrix breakdown with failure to repair. Disease mechanisms and therapeutic interventions appear to coincide in both exposure scenarios. One of the more widely applied interventions, the anti-oxidant therapy, is successful for both mainstream and SHS. The comparison of direct with indirect smoke exposure studies in this review emphasizes that, even though there are many overlapping pathways, it is not conclusive that SHS is using exactly the same mechanisms as direct smoke in COPD pathogenesis, but should be considered a preventable health risk. Some characteristics and therapeutic alternatives uniquely exist in SHS-related COPD.
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影响因子：
4.7
作者：
Balansky, RM;D'Agostini, F;De Flora, S
通讯作者：
De Flora, S
影响因子：
5.8
作者：
Braber S;Henricks PA;Nijkamp FP;Kraneveld AD;Folkerts G
通讯作者：
Folkerts G
影响因子：
9.6
作者：
Berglund, DJ;Abbey, DE;McDonnell, WF
通讯作者：
McDonnell, WF
影响因子：
24.3
作者：
Bartalesi, B;Cavarra, E;Lungarella, G
通讯作者：
Lungarella, G
DOI：
10.1165/rcmb.2007-0295oc
发表时间：
2008-10-01
影响因子：
6.4
作者：
Adair-Kirk, Tracy L.;Atkinson, Jeffrey J.;Betsuyaku, Tomoko
通讯作者：
Betsuyaku, Tomoko