Pathogenic mechanism of second hand smoke induced inflammation and COPD.
Pathogenic mechanism of second hand smoke induced inflammation and COPD.
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DOI：
10.3389/fphys.2012.00348
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发表时间：
2012
影响因子：
4
通讯作者：
Di YP
中科院分区：
文献类型：
--
作者：
Birru RL;Di YP
二手烟（SHS）将数千种有毒化学物质引入肺中，包括致癌物质和氧化剂，这些物质会导致直接的气道上皮组织破坏。它还可以通过其对与组织细胞修复相关的信号传导途径的影响以及通过异常诱导炎症进入肺部而引起间接损害。反复暴露于SHS后，这些症状可导致肺部炎症性疾病的发展，包括慢性阻塞性肺病（COPD）。COPD是一种严重的肺部疾病，其特征在于慢性炎症和不可逆的组织破坏。目前还没有治愈的病因，因为疾病发展和进展背后的机制仍然未知。最近的发现表明，与炎症反应相关的遗传易感性有助于COPD的发展，与不规则的先天和适应性免疫有关，也是癌症的危险因素。使用动物模型进行香烟烟雾（CS）和SHS相关的体内实验，在阐明COPD炎症相关发展的致病机制和遗传成分方面至关重要。
Second hand smoke (SHS) introduces thousands of toxic chemicals into the lung, including carcinogens and oxidants, which cause direct airway epithelium tissue destruction. It can also illicit indirect damage through its effect on signaling pathways related to tissue cell repair and by the abnormal induction of inflammation into the lung. After repeated exposure to SHS, these symptoms can lead to the development of pulmonary inflammatory disorders, including chronic obstructive pulmonary disease (COPD). COPD is a severe pulmonary disease characterized by chronic inflammation and irreversible tissue destruction. There is no causal cure, as the mechanism behind the development and progression of the disease is still unknown. Recent discoveries implicate genetic predisposition associated with inflammatory response contributed to the development of COPD, linked to irregular innate and adaptive immunity, as well as a risk factor for cancer. The use of animal models for both cigarette smoke (CS) and SHS associated in vivo experiments has been crucial in elucidating the pathogenic mechanisms and genetic components involved in inflammation-related development of COPD.
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影响因子：
3.4
作者：
Guo, Yi;Gong, Yi;Wan, Huanying
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DOI：
10.1164/ajrccm/144.3_pt_1.570
发表时间：
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期刊：
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作者：
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