PULMONARY SURFACTANT SYSTEM AND RADIATION PNEUMONITIS

肺纤维化和肺炎是相互关联的，代表着 放射性肺损伤的表达谱。尽管漫射 肺炎是一种更戏剧性的和相对早期的事件，在中毒之后 剂量的辐射，纤维化的过程是致命的或衰弱的 尽管是后来的事。无论在临床上还是在实验室里，都有广泛的 已经研究了各种剂量/时间分级计划，并已 导致了肺炎和纤维化的两个过程 是由于不同的靶细胞，即II型上皮细胞和 间隔成纤维细胞，在时间上是不同的 反应的表达式。从我们自己的调查中获得的新证据 正如其他人所暗示的那样，这是一个多细胞的过程 以及通过相互沟通来维持纤维化过程 在不同的肺细胞之间。也就是说，在辐射后不久， 多种生长和抑制因子的合成和分泌 在之后的所谓“潜伏期”期间，这种情况会持续几周到几个月 致命的暴露。事实上，损伤的基因表达很可能 在数小时和/或数天内立即发生，因为存在遗传事件 它们控制和调节信号和受体的释放， 控制事件的动态顺序。对目标的简要总结 放射损伤的细胞被用来阐明病理生理学。 事件和假设的生物标记物，即生化和 增长因素。 对辐射损伤的反应是一个复杂的过程，需要 从新的分子生理学角度进行研究以解释 组织病理学事件。单个目标单元的概念可以 解释在致命事件之后发生的动态事件序列 肺照射被多细胞系统的照射所取代 互动。所谓的“潜伏期”为数周或数月 辐射反应正在被自我分泌的升值所取代， 旁分泌和内分泌信息在手术后立即发送 受到多种细胞的照射：上皮细胞， 内皮细胞、成纤维细胞和巨噬细胞。《公约》 这个过程是通过对细胞周期的遗传重新编程，一种 生长因子和抑制因子的变化 接收这些信号的特定细胞受体，以及由此产生的 这些信号在受体后的转导和翻译 胞质、核和间质事件。

Pulmonary fibrosis and pneumonitis are inter-related and represent the spectrum of expression of lung injury to irradiation. Although a diffuse pneumonitis is a more dramatic and relatively early event following toxic doses of radiation, the fibrotic process is as lethal or debilitating albeit a later event. Both in the clinic and in the laboratory, a wide variety of dose/time fractionation schedules have been studied and have led to the proposition that the two processes of pneumonitis and fibrosis are due to different target cells, i.e. type II epithelial cells and the septal fibroblast respectively and are distinct in time as to the expression of the reaction. New evidence from our own investigations as well as others suggests this is a multicellular process with initiation and sustaining of the fibrogenic process through an intercommunication between different lung cells. That is, soon after irradiation there is the synthesis and secretion of numerous growth and inhibitory factors that occur for weeks to months during the so-called "latent" period after a lethal exposure. In fact, the genetic expression of injury probably occurs immediately, within hours and/or days, as there are genetic events which control and regulate the release of signals and receptors and control the dynamic sequence of events. A concise summary of target cells injured by irradiation is presented to clarify the pathophysiologic events and the hypothesized biological markers, i.e. biochemical and growth factors. The response to radiation injury is a complex process and needs to be investigated in terms of the new molecular physiology to explain the histopathologic events. The concept of a single target cell which can explain the dynamic sequence of events which occurs following lethal pulmonary irradiation is supplanted by that of multiple cell systems interacting. The so-called "latent" period of weeks or months to express radiation reactions is being replaced by appreciation of autocrine, paracrine and endocrine messages being sent immediately after the injurious exposure to irradiation by a variety of cells: epithelial, endothelial, fibroblasts and macrophages. The implementation of the process is by genetic reprogramming of the cell cycle, the response of a variety of growth factors and inhibiting factors, the alteration of specific cell receptors to receive these signals, and the resulting transduction and translation of these signals into post receptor cytoplasmic, nuclear and interstitial events.