Lebedeva E S, Kuzubova N A, Danilov L N, Titova O N, Dvorakovskaya I V, Kozlova M Ya, Preobrazhenskaya T N, Platonova I S
Institute of Pulmonology, I. P. Pavlov State Medical University, St. Petersburg, Russia.
Bull Exp Biol Med. 2012 Mar;152(5):659-63. doi: 10.1007/s10517-012-1601-3.
A method for experimental reproduction of stages of chronic obstructive pulmonary disease formation (from acute inflammation to bronchopulmonary tissue restructuring characteristic of this disease) is presented. Lung injury and inflammation were induced by nitrogen dioxide. Hyperplasia and hypersecretion of goblet cells, squamous cell metaplasia of the ciliary epithelium, emphysema, and focal fibrosis served as the morphological substrate for the formation of bronchial obstruction. The adequacy of the model is confirmed by signs characteristic of chronic obstructive pulmonary disease: hyperexpression of CD3 lymphocytes in the bronchial wall and parenchyma, manifold increased production of TNFα and TGFβ, high concentrations of circulating pathogenic immune complexes. Persistence of the structural and functional shifts throughout 6 months after exposure to nitrogen dioxide indicated a chronic course of the resultant pathological process.
本文提出了一种用于实验性再现慢性阻塞性肺疾病形成阶段（从急性炎症到该疾病特有的支气管肺组织重塑）的方法。通过二氧化氮诱导肺损伤和炎症。杯状细胞增生和分泌亢进、纤毛上皮鳞状化生、肺气肿和局灶性纤维化是支气管阻塞形成的形态学基础。该模型的充分性通过慢性阻塞性肺疾病的特征性体征得到证实：支气管壁和实质中CD3淋巴细胞的过度表达、TNFα和TGFβ的大量增加产生、循环致病性免疫复合物的高浓度。在接触二氧化氮后6个月内结构和功能变化持续存在，表明所产生的病理过程为慢性病程。
