Dziedzic D, Wright E S, Sargent N E
General Motors Research Laboratories, Biomedical Science Department, Warren, Michigan 48090-9055.
Environ Res. 1990 Apr;51(2):194-208. doi: 10.1016/s0013-9351(05)80089-1.
The purpose of this work is to assess the effect of ozone, a reactive product of environmental photochemical oxidation, on lymphocytes of the lung. We exposed male Fischer rats to ozone at a concentration of 0.5 ppm for 20 hr/day for 1-14 days. Animals were treated with radioactive thymidine and were sacrificed at Day 1, 2, 3, 7, or 14 of exposure. Lungs and mediastinal lymph nodes were removed and prepared for histologic examination, evaluation of labeling indexes, and morphometric measurement. We examined two components of the lymphocyte response of the lung: the airway-related response, represented by the reaction of the bronchus-associated lymphoid tissue (BALT), and the deep lung-related response, represented by reaction of the mediastinal lymph node. Lymphocytes of both the BALT and the mediastinal lymph node showed elevated radioactive thymidine uptake; however, no evidence of cell death was observed at either site. The cells of the specialized epithelium covering the BALT (lymphoepithelium) showed increased vacuolization, indicating altered cellular function. The average size of BALTs was unchanged by ozone exposure. Under experimental conditions ozone can affect a variety of cells in the lung including bronchial epithelial cells, macrophages, and Type 1 cells. We have shown for the first time that in addition to these cells, the rat BALT also proliferates in response to ozone. In addition we confirm previous work in the mouse which shows that the mediastinal lymph node reacts as well. The airways can be affected by inflammation, can be targets of infection, and can respond to chemical irritants with bronchoconstrictive responses. They are an important target organ for hypersensitivity responses and are a primary site for pulmonary cancer formation. A role for lymphocytes has been implicated in each of these processes. Therefore, the clinical significance of ozone on BALT and mediastinal lymph node responses could be appreciable in terms of potentiation of, or protection against, such responses.
本研究旨在评估环境光化学氧化反应产物臭氧对肺淋巴细胞的影响。我们将雄性Fischer大鼠暴露于浓度为0.5 ppm的臭氧环境中，每天暴露20小时，持续1 - 14天。给动物注射放射性胸腺嘧啶核苷，并在暴露的第1、2、3、7或14天处死。取出肺和纵隔淋巴结，准备进行组织学检查、标记指数评估和形态测量。我们研究了肺淋巴细胞反应的两个组成部分：以支气管相关淋巴组织（BALT）反应为代表的气道相关反应，以及以纵隔淋巴结反应为代表的深部肺相关反应。BALT和纵隔淋巴结中的淋巴细胞均显示放射性胸腺嘧啶核苷摄取增加；然而，在这两个部位均未观察到细胞死亡的证据。覆盖BALT的特殊上皮细胞（淋巴上皮）出现空泡化增加，表明细胞功能改变。臭氧暴露未改变BALT的平均大小。在实验条件下，臭氧可影响肺内多种细胞，包括支气管上皮细胞、巨噬细胞和I型细胞。我们首次表明，除这些细胞外，大鼠BALT也会对臭氧产生增殖反应。此外，我们证实了先前在小鼠中的研究结果，即纵隔淋巴结也会产生反应。气道可受到炎症影响，可成为感染靶点，并可对化学刺激物产生支气管收缩反应。它们是超敏反应的重要靶器官，也是肺癌形成的主要部位。淋巴细胞在上述每个过程中都发挥了作用。因此，臭氧对BALT和纵隔淋巴结反应的临床意义在增强或预防此类反应方面可能相当显著。
