The role of pro- and anti-inflammatory responses in silica-induced lung fibrosis.
The role of pro- and anti-inflammatory responses in silica-induced lung fibrosis.
复制标题
促疾病和抗炎反应在二氧化硅诱导的肺纤维化中的作用。
DOI：
10.1186/1465-9921-6-112
复制
发表时间：
2005-10-07
影响因子：
5.8
通讯作者：
Huaux F
中科院分区：
文献类型：
--
作者：
Barbarin V;Nihoul A;Misson P;Arras M;Delos M;Leclercq I;Lison D;Huaux F
人们普遍认为慢性炎症是肺纤维化的必要组成部分，但这一概念最近受到质疑。使用生物化学、组织学、免疫组织化学和细胞分析，我们比较了Sprague-Dawley大鼠和NMRI小鼠对致纤维化二氧化硅颗粒（2.5和25 mg/g肺）的肺反应（炎症和纤维化）。用二氧化硅颗粒处理的大鼠出现慢性和进行性炎症，伴有TNF-α过度产生以及严重的肺纤维化。地塞米松或吡格列酮限制了大鼠对二氧化硅的肺纤维化反应的幅度，支持炎症驱动肺纤维化的范例。与此形成鲜明对比的是，在小鼠中，二氧化硅仅诱导了有限和短暂的炎症，而没有TNF-α过度产生。然而，小鼠的肺纤维化程度与大鼠相似。小鼠的纤维化反应伴随着二氧化硅活化的肺巨噬细胞的抗炎和纤维化细胞因子IL-10的高表达。在小鼠中，IL-10仅由纤维化颗粒诱导，并且在二氧化硅敏感但不耐二氧化硅的小鼠品系的肺中显著表达。抗炎治疗不能控制小鼠的肺纤维化。这些结果表明，除了慢性肺部炎症外，显著的抗炎反应也可能有助于二氧化硅诱导的肺纤维化的扩展，并代表导致肺纤维化的替代途径。
It has been generally well accepted that chronic inflammation is a necessary component of lung fibrosis but this concept has recently been challenged. Using biochemical, histological, immunohistochemistry, and cellular analyses, we compared the lung responses (inflammation and fibrosis) to fibrogenic silica particles (2.5 and 25 mg/g lung) in Sprague-Dawley rats and NMRI mice. Rats treated with silica particles developed chronic and progressive inflammation accompanied by an overproduction of TNF-α as well as an intense lung fibrosis. Dexamethasone or pioglitazone limited the amplitude of the lung fibrotic reaction to silica in rats, supporting the paradigm that inflammation drives lung fibrosis. In striking contrast, in mice, silica induced only a limited and transient inflammation without TNF-α overproduction. However, mice developed lung fibrosis of a similar intensity than rats. The fibrotic response in mice was accompanied by a high expression of the anti-inflammatory and fibrotic cytokine IL-10 by silica-activated lung macrophages. In mice, IL-10 was induced only by fibrotic particles and significantly expressed in the lung of silica-sensitive but not silica-resistant strains of mice. Anti-inflammatory treatments did not control lung fibrosis in mice. These results indicate that, beside chronic lung inflammation, a pronounced anti-inflammatory reaction may also contribute to the extension of silica-induced lung fibrosis and represents an alternative pathway leading to lung fibrosis.
登录
查看更多内容
影响因子：
1.7
作者：
Blake, TL;Dimatteo, M;Reasor, MJ
通讯作者：
Reasor, MJ
DOI：
10.1152/ajplung.00433.2003
发表时间：
2004-09-01
影响因子：
4.9
作者：
Kim, J;McKinley, L;Remick, DG
通讯作者：
Remick, DG
DOI：
10.1152/ajplung.2000.278.5.l914
发表时间：
2000-05-01
影响因子：
4.9
作者：
Arai, T;Abe, K;Hayashi, S
通讯作者：
Hayashi, S
影响因子：
4.4
作者：
Huaux, F;Arras, M;Lison, D
通讯作者：
Lison, D
DOI：
10.1165/ajrcmb.20.4.3342
发表时间：
1999-04-01
影响因子：
6.4
作者：
Huaux, F;Lardot, C;Lison, D
通讯作者：
Lison, D