Bellum S C, Hamamdzic D, Thompson A H, Harley R A, London S D, London L
Department of Microbiology and Immunology, Medical University of South Carolina, Charleston 29425, USA.
Lab Invest. 1996 Jan;74(1):221-31.
A number of studies have examined the nature of the respiratory immune response to particular pathogens. Although many pathogens stimulate specific immunity in the lung, they frequently are not effective immunogens at other mucosal sites. Because the gastrointestinal tract is a major inductive site for mucosal immunity, a pathogen that is an effective respiratory and gut immunogen would allow studies of the interaction of the lung with gut mucosal immune system. Reovirus, a respiratory isolate that previously has been shown to be an effective gut mucosal immunogen, provides a potential model of the relationship of the lung to the gut mucosal immune system. In this report, we demonstrate that intranasal application of reovirus serotype 1/strain Lang (1/L) to CD-1 mice elicits an acute lymphocytic inflammatory infiltration of the lung and hyperplasia of the lung-associated lymph nodes. The initial inflammatory response occurs in the airspaces and interstitium of the lung. As the infection progresses, the initially diffuse cellular infiltrate becomes more focused around small bronchioles. Viral replication occurs predominantly during the first week of the infection, and infectious virions are eliminated during the second week. After the elimination of infectious virions, a secondary response consisting of the appearance of plasma cells adjacent to pulmonary arteries develops as the primary infiltrate organizes into peribronchiolar follicles, resembling the human inflammatory lung condition termed follicular bronchiolitis. These two infiltration patterns were also observed by immunohistochemical analysis of the the infected lung. Whereas CD4+ and CD8+ lymphocytes and Mac-1+ cells were found to be more closely associated with the primary infiltration process, B220+ lymphocytes were observed adjacent to pulmonary arteries. These results establish respiratory reovirus 1/L infection as a viable model for future investigations of the mucosal immune response in the lung and its relationship to the common mucosal immune system.
多项研究探讨了针对特定病原体的呼吸道免疫反应的性质。尽管许多病原体可刺激肺部的特异性免疫，但它们在其他黏膜部位往往不是有效的免疫原。由于胃肠道是黏膜免疫的主要诱导部位，一种既是有效的呼吸道免疫原又是肠道免疫原的病原体，将有助于研究肺部与肠道黏膜免疫系统之间的相互作用。呼肠孤病毒是一种呼吸道分离株，此前已被证明是一种有效的肠道黏膜免疫原，它为研究肺部与肠道黏膜免疫系统的关系提供了一个潜在模型。在本报告中，我们证明将1型呼肠孤病毒朗株（1/L）经鼻应用于CD-1小鼠可引发肺部急性淋巴细胞炎性浸润以及肺相关淋巴结增生。最初的炎症反应发生在肺的气腔和间质。随着感染进展，最初弥漫性的细胞浸润变得更加集中在小支气管周围。病毒复制主要发生在感染的第一周，感染性病毒粒子在第二周被清除。在感染性病毒粒子被清除后，随着主要浸润组织形成支气管周围滤泡，一种由肺动脉旁浆细胞出现组成的二次反应开始出现，类似于人类称为滤泡性细支气管炎的炎性肺部疾病。通过对感染肺组织的免疫组化分析也观察到了这两种浸润模式。虽然发现CD4+和CD8+淋巴细胞以及Mac-1+细胞与初次浸润过程关系更为密切，但在肺动脉旁观察到了B220+淋巴细胞。这些结果确立了呼吸道呼肠孤病毒1/L感染作为未来研究肺部黏膜免疫反应及其与共同黏膜免疫系统关系的可行模型。
