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首页> 外文期刊>Infection and immunity >Diminished ICAM-1 Expression and Impaired Pulmonary Clearance of Nontypeable Haemophilus influenzae in a Mouse Model of Chronic Obstructive Pulmonary Disease/Emphysema
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Diminished ICAM-1 Expression and Impaired Pulmonary Clearance of Nontypeable Haemophilus influenzae in a Mouse Model of Chronic Obstructive Pulmonary Disease/Emphysema

机译：在慢性阻塞性肺疾病/肺气肿的小鼠模型中ICAM-1表达降低和不可分型流感嗜血杆菌的肺通透性受损

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The airways of patients with chronic obstructive pulmonary disease (COPD) are continually colonized with bacterial opportunists like nontypeable Haemophilus influenzae (NTHi), and a wealth of evidence indicates that changes in bacterial populations within the lung can influence the severity of COPD. In this study, we used a murine model for COPD/emphysema to test the hypothesis that COPD affects pulmonary clearance. Mice were treated with a pulmonary bolus of elastase, and as reported previously, the lungs of these mice were pathologically similar to those with COPD/emphysema at ～1 month posttreatment. Pulmonary clearance of NTHi was significantly impaired in elastase-treated versus mock-treated mice. While histopathologic analysis revealed minimal differences in localized lung inflammation between the two groups, lower levels of intercellular adhesion molecule 1 (ICAM-1) were observed for the airway epithelial surface of elastase-treated mice than for those of control mice. Following infection, elastase-treated mice had lung pathology consistent with pneumonia for as long as 72 h postinfection, whereas at the same time point, mock-treated mice had cleared NTHi and showed little apparent pathology. Large aggregates of bacteria were observed within damaged lung tissue of the elastase-treated mice, whereas sparse individual bacteria were observed in lungs of mock-treated mice at the same time point postinfection. Additional infection studies showed that NTHi mutants with biofilm defects were less persistent in the elastase-treated mice than the parent strain. These findings establish a model for COPD-related infections and support the hypotheses that ICAM-1 promotes clearance of NTHi. Furthermore, the data indicate that NTHi may form biofilms within the context of COPD-related infections.
机译：慢性阻塞性肺疾病（COPD）患者的气道不断被细菌型机会主义者如不可分型的流感嗜血杆菌（emHi）（NTHi）所定植，大量证据表明，肺内细菌种群的变化会影响肺炎的发生。 COPD的严重程度。在这项研究中，我们使用了针对COPD /肺气肿的小鼠模型来检验COPD影响肺部清除率的假设。小鼠经肺弹性蛋白酶推注治疗，如先前报道，在治疗后约1个月，这些小鼠的肺在病理学上与COPD /肺气肿相似。与经模拟处理的小鼠相比，经弹性蛋白酶处理的小鼠的NTHi的肺部清除能力显着受损。虽然组织病理学分析显示两组之间的局部肺部炎症差异最小，但弹性蛋白酶处理小鼠的气道上皮表面的细胞间粘附分子1（ICAM-1）水平低于对照组。感染后，经弹性蛋白酶处理的小鼠感染后长达72小时的肺部病理与肺炎一致，而在同一时间点，经模拟处理的小鼠已清除NTHi，几乎没有明显的病理。在弹性蛋白酶处理的小鼠的受损肺组织中观察到大量细菌聚集，而在感染后同一时间在模拟处理的小鼠的肺中观察到稀疏的单个细菌。进一步的感染研究表明，在用弹性蛋白酶处理的小鼠中，具有生物膜缺陷的NTHi突变体比亲本菌株的持久性较低。这些发现建立了COPD相关感染的模型，并支持ICAM-1促进NTHi清除的假设。此外，数据表明NTHi可能在COPD相关感染的背景下形成生物膜。

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