Amplification of inflammation in emphysema and its association with latent adenoviral infection
Amplification of inflammation in emphysema and its association with latent adenoviral infection
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DOI：
10.1164/ajrccm.164.3.2007149
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发表时间：
2001-08-01
影响因子：
24.7
通讯作者：
Hogg, JC
中科院分区：
文献类型：
--
作者：
Retamales, I;Elliott, WM;Hogg, JC
本研究检验了严重肺气肿中香烟引起的炎症过程被放大的假设，并探讨了这种反应与潜伏腺病毒感染的关系。肺切除术获得无（n = 7）、轻度（n = 7）或重度肺气肿（n = 7）的相似吸烟史患者的肺组织。使用定量技术测定组织和空气中存在的多形核细胞（PMN）、巨噬细胞、B细胞、CD4、CD8淋巴细胞和嗜酸性粒细胞以及表达腺病毒E1A蛋白的上皮细胞的数量。严重肺气肿与肺组织和空气中炎症细胞总数的绝对增加有关。计算机断层扫描（CT）确定的肺破坏程度与组织中细胞数/m(2)表面积的R-2值相关，R-2值范围为0.858 （CD8细胞）至0.483 （B细胞），空气中细胞数范围为0.630 （CD4细胞）至0.198 （B细胞）。这些变化分别与轻度和重度疾病中表达腺病毒EIA蛋白的肺泡上皮细胞数量增加5- 40倍有关。我们得出结论，香烟引起的肺部炎症在严重肺气肿中被放大，肺泡上皮细胞表达的腺病毒E1A蛋白的潜在表达影响了这一放大过程。
This study examines the hypothesis that the cigarette smoke-induced inflammatory process is amplified in severe emphysema and explores the association of this response with latent adenoviral infection. Lung tissue from patients with similar smoking histories and either no (n = 7), mild (n = 7), or severe emphysema (n = 7) was obtained by lung resection. Numbers of polymorphonuclear cells (PMN), macrophages, B cells, CD4, CD8 lymphocytes, and eosinophils present in tissue and airspaces and of epithelial cells expressing adenoviral E1A protein were determined using quantitative techniques. Severe emphysema was associated with an absolute increase in the total number of inflammatory cells in the lung tissue and airspaces. The computed tomography (CT) determined extent of lung destruction was related to the number of cells/m(2) surface area by R-2 values that ranged from 0.858 (CD8 cells) to 0.483 (B cells) in the tissue and 0.630 (CD4 cells) to 0.198 (B cells) in the airspaces. These changes were associated with a 5- to 40-fold increase in the number of alveolar epithelial cells expressing adenoviral EIA protein in mild and severe disease, respectively. We conclude that cigarette smoke-induced lung inflammation is amplified in severe emphysema and that latent expression of the adenoviral E1A protein expressed by alveolar epithelial cells influenced this amplification process.