Yoshizawa Y, Hostetter M W, Nakazawa T, Ripani L M, Dawson C A, Moore V L
J Lab Clin Med. 1982 Jul;100(1):61-9.
Intrapulmonary instillation of proteins into rabbit lungs with BCG-induced granulomatous inflammation results in greater transport of these molecules into the blood, and the primary route is probably the pulmonary lymphatics. In addition, rabbits with inflamed lungs develop a more potent systemic immune response when exposed to soluble antigens as an aerosol. The current study was done to further study the mechanisms of this phenomenon using the Jerne plaque technique. Intrapulmonary immunization with soluble antigens (solubilized SRBCs and HSA) resulted in a greater PFC response to both antigens when the lungs exhibited BCG-induced granulomatous inflammation. A previous study demonstrated that more antigen administered intratracheally was found in the HLNs when the lungs displayed granulomatous inflammation. However, in the present study, we did not observe an enhanced PFC response in HLN cells when antigens were introduced into inflamed lungs. When rabbits with BCG-inflamed lungs were immunized i.v., they did not develop an enhanced PFC response in the spleen. Immunization into the respiratory tract of normal rabbits with large doses (300 micrograms) of soluble antigens also resulted in a substantial PFC response in the spleen that was quantitatively greater than that induced by the same i.v. dose. These data indicate that (1) administration of antigens into inflamed lung results in an enhanced systemic immune response, (2) although larger quantities of soluble antigens administered by the pulmonary route accumulate in the HLN when lungs are inflamed, cells from this tissue do not exhibit an enhanced PFC response, and (3) large doses of soluble antigens instilled into normal lungs induce a greater systemic immune response that the same doses administered i.v. This study further demonstrates the importance of pulmonary inflammation and the immune response to inhaled antigens and provides insight as to how individuals with chronic inflammatory lung disease can react in an augmented fashion to environmental antigens.
将蛋白质经肺内注入卡介苗诱导产生肉芽肿性炎症的兔肺中，会使这些分子更多地转运至血液中，其主要途径可能是肺淋巴管。此外，肺部发炎的兔子在接触作为气雾剂的可溶性抗原时，会产生更强的全身免疫反应。本研究旨在利用耶尔恩斑技术进一步探究这一现象的机制。当肺部表现出卡介苗诱导的肉芽肿性炎症时，经肺内用可溶性抗原（溶解的绵羊红细胞和人血清白蛋白）免疫会导致对这两种抗原产生更强的空斑形成细胞（PFC）反应。先前的一项研究表明，当肺部出现肉芽肿性炎症时，经气管内给予的更多抗原会在肺门淋巴结（HLN）中被发现。然而，在本研究中，当将抗原引入发炎的肺部时，我们并未观察到HLN细胞中的PFC反应增强。当对卡介苗致肺部发炎的兔子进行静脉免疫时，它们在脾脏中并未产生增强的PFC反应。用大剂量（300微克）可溶性抗原对正常兔子进行呼吸道免疫，也会在脾脏中产生大量的PFC反应，其数量上比相同静脉剂量诱导的反应更大。这些数据表明：（1）将抗原注入发炎的肺部会导致全身免疫反应增强；（2）尽管当肺部发炎时经肺途径给予的大量可溶性抗原会在HLN中积聚，但来自该组织的细胞并未表现出增强的PFC反应；（3）将大剂量可溶性抗原注入正常肺部所诱导的全身免疫反应比相同剂量静脉注射时更强。本研究进一步证明了肺部炎症以及对吸入抗原的免疫反应的重要性，并为患有慢性炎症性肺病的个体如何以增强的方式对环境抗原作出反应提供了见解。
