Nakayama Y, Makino S, Fukuda Y, Min K Y, Shimizu A, Ohsawa N
First Department of Internal Medicine, Osaka Medical College, Japan.
Int J Radiat Oncol Biol Phys. 1996 Jan 15;34(2):459-67. doi: 10.1016/0360-3016(95)02101-9.
Radiation pneumonitis sometimes extends beyond the irradiated area of a lung and can also affect the opposite lung. Some immunological mechanisms, in addition to simple direct injury of the lungs by radiation, seem to be involved in the onset of radiation pneumonitis. To clarify such mechanisms, the effects of radiation on local inflammatory cells in lungs, in particular, lymphocytes, were examined.
A comparison was made of bronchoalveolar lavage fluid (BALF) findings from 13 irradiated patients (RT group) and 15 nonirradiated patients (non-RT group) with lung cancer. Patients who later developed radiation pneumonitis (RP group) and those who did not (RP-free group) were also compared. Using a two-color flowcytometer, radiation-induced changes in local inflammatory cells in lungs were analyzed. This included analyses of human leukocyte-associated antigen (HLADR) and intercellular adhesion molecule-1 (ICAM-1) expression on T-cells, which are though to be involved in cell activation and interactions between cells.
The following aspects of BALF were higher in the RT group than in the non-RT group: (a) the percentage of lymphocytes and eosinophiles; (b) the incidence of HLADR-positive CD4+T-cells and HLADR-positive CD8+T-cells; and (c) the incidence of ICAM-1--positive T-cells. The following aspects of BALF were higher in the RP group than in the RP-free group: (a) the total cell counts; (b) the percentage of lymphocytes; and (c) the incidence of ICAM-1-positive T-cells. A significant relationship was seen between the incidence of ICAM-1 expression on T-cells and the number of days from the initiation of radiotherapy to the onset of radiation pneumonitis.
These data suggest that irradiation can induce accumulation of activated T-cells (HLADR and ICAM-1--positive T-cells) in the lung. This accumulation may be closely linked to radiation-induced lung injury. It is also suggested that the incidence of ICAM-1--positive T-cells in BALF may serve as a useful clinical marker of radiation pneumonitis.
放射性肺炎有时会超出肺部受照射区域,还可能影响对侧肺。除了辐射对肺的简单直接损伤外,一些免疫机制似乎也参与了放射性肺炎的发病过程。为阐明这些机制,研究了辐射对肺局部炎症细胞,尤其是淋巴细胞的影响。
比较了13例接受放疗的肺癌患者(放疗组)和15例未接受放疗的肺癌患者(非放疗组)的支气管肺泡灌洗(BALF)结果。还比较了后来发生放射性肺炎的患者(RP组)和未发生放射性肺炎的患者(无RP组)。使用双色流式细胞仪分析辐射诱导的肺局部炎症细胞变化。这包括分析人类白细胞相关抗原(HLADR)和细胞间黏附分子-1(ICAM-1)在T细胞上的表达,这些被认为与细胞活化和细胞间相互作用有关。
放疗组BALF的以下方面高于非放疗组:(a)淋巴细胞和嗜酸性粒细胞百分比;(b)HLADR阳性CD4+T细胞和HLADR阳性CD8+T细胞的发生率;(c)ICAM-1阳性T细胞的发生率。RP组BALF的以下方面高于无RP组:(a)细胞总数;(b)淋巴细胞百分比;(c)ICAM-1阳性T细胞的发生率。T细胞上ICAM-1表达的发生率与放疗开始至放射性肺炎发病的天数之间存在显著关系。
这些数据表明,辐射可诱导活化T细胞(HLADR和ICAM-1阳性T细胞)在肺中积聚。这种积聚可能与辐射诱导的肺损伤密切相关。还表明,BALF中ICAM-1阳性T细胞的发生率可能是放射性肺炎的一个有用临床标志物。