Lung fibrotic responses to particle exposure
Lung fibrotic responses to particle exposure
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DOI：
10.1080/01926230601060009
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发表时间：
2007-01-01
影响因子：
1.5
通讯作者：
Bonner, James C.
中科院分区：
文献类型：
--
作者：
Bonner, James C.
许多人为来源产生的颗粒物有可能导致或加重肺部疾病，包括哮喘、支气管炎和COPD。纤维化反应是所有这些肺部疾病的组成部分，并且涉及肺成纤维细胞胶原蛋白的进行性沉积。肺中颗粒的反应性、毒性和纤维化潜力取决于多种因素，包括颗粒大小、表面积和组成。较小的颗粒，特别是在纳米尺寸范围内，由于较高的表面质量比和较大的氧化剂生成潜力，具有更大的毒性和纤维化能力。组成也是对颗粒的纤维化反应的重要决定因素。过渡金属、细菌脂多糖和多环芳烃是颗粒的一些毒性组分，其激活细胞内信号传导途径，最终导致促纤维化细胞因子和生长因子的产生。
Particles generated from numerous anthropogenic sources have the potential to cause or exacerbate lung diseases, including asthma, bronchitis, and COPD. Fibrotic reactions are a component of all of these pulmonary diseases, and involve the progressive deposition of collagen by pulmonary fibroblasts. The reactivity, toxicity, and fibrogenic potential of particles in the lung depends on a variety of factors including particle size, surface area, and composition. Smaller particles, particularly in the nanosized range, have more toxic and fibrogenic capacity due to a higher surface-to-mass ratio and greater oxidant- generating potential. Composition is also an important determinant in the fibrotic response to particles. Transition metals, bacterial lipopolysaccaride, and polycyclic aromatic hydrocarbons are some of the toxic components of particles that activate intracellular signaling pathways that culminate in the production of profibrotic cytokines and growth factors.