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首页> 外文期刊>American Journal of Physiology >Endotoxin responsiveness and subchronic grain dust-induced airway disease.
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Endotoxin responsiveness and subchronic grain dust-induced airway disease.

机译：内毒素反应性和亚慢性谷物粉尘诱发的气道疾病。

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摘要

Endotoxin is one of the principal components of grain dust that causes acute reversible airflow obstruction and airway inflammation. To determine whether endotoxin responsiveness influences the development of chronic grain dust-induced airway disease, physiological and airway inflammation remodeling parameters were evaluated after an 8-wk exposure to corn dust extract (CDE) and again after a 4-wk recovery period in a strain of mice sensitive to (C3H/HeBFeJ) and one resistant to (C3H/HeJ) endotoxin. After the CDE exposure, both strains of mice had equal airway hyperreactivity to a methacholine challenge; however, airway hyperreactivity persisted only in the C3H/HeBFeJ mice after the recovery period. Only the C3H/HeBFeJ mice showed significant inflammation of the lower airway after the 8-wk exposure to CDE. After the recovery period, this inflammatory response completely resolved. Lung stereological measurements indicate that an 8-wk exposure to CDE resulted in persistent expansion of the airway submucosal cross-sectional area only in the C3H/HeBFeJ mice. Collagen type III and an influx of cells into the subepithelial area participated in the expansion of the submucosa. Our findings demonstrate that subchronic inhalation of grain dust extract results in the development of chronic airway disease only in mice sensitive to endotoxin but not in mice that are genetically hyporesponsive to endotoxin, suggesting that endotoxin is important in the development of chronic airway disease.
机译：内毒素是谷物粉尘的主要成分之一，可导致急性可逆性气流阻塞和气道炎症。为了确定内毒素反应性是否影响慢性谷物粉尘诱发的气道疾病的发生，在菌株中玉米粉尘提取物（CDE）暴露8周后和菌株恢复4周后再次评估生理和气道炎症重塑参数对（C3H / HeBFeJ）敏感的小鼠和对（C3H / HeJ）内毒素有抗性的小鼠。 CDE暴露后，两种品系的小鼠对乙酰甲胆碱攻击均具有相同的气道高反应性。但是，恢复期后，气道高反应性仅在C3H / HeBFeJ小鼠中持续存在。在8周暴露于CDE之后，只有C3H / HeBFeJ小鼠表现出下呼吸道的明显炎症。恢复期过后，这种炎症反应完全消失了。肺部立体测量结果表明，仅在C3H / HeBFeJ小鼠中，8周暴露于CDE会导致气道粘膜下横断面区域持续扩展。 III型胶原蛋白和细胞流入上皮下区域参与了粘膜下层的扩张。我们的研究结果表明，亚慢性吸入谷物粉尘提取物只会在对内毒素敏感的小鼠中导致慢性气道疾病的发展，而不会在对内毒素遗传上反应低的小鼠中导致慢性气道疾病的发展，这表明内毒素在慢性气道疾病的发展中很重要。

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