Pathogenesis of Pulmonary Tuberculosis: an Interplay of Tissue-Damaging and Macrophage-Activating Immune Responses—Dual Mechanisms That Control Bacillary Multiplication
Pathogenesis of Pulmonary Tuberculosis: an Interplay of Tissue-Damaging and Macrophage-Activating Immune Responses—Dual Mechanisms That Control Bacillary Multiplication
复制标题
肺结核的发病机制：组织损伤和巨噬细胞激活免疫反应的相互作用——控制细菌增殖的双重机制
DOI：
--
复制
发表时间：
1994
期刊：
影响因子：
--
通讯作者：
G. Rook
中科院分区：
文献类型：
--
作者：
A. Dannenberg;G. Rook
一旦建立了第一个小的干酪性结核病变，所有随后的战斗都发生在能够破坏组织和激活巨噬细胞的免疫反应的宿主中。破坏组织和激活巨噬细胞的免疫反应都可以阻止结核杆菌的生长(即增殖)，因为这些杆菌在非液化的干酪坏死组织中不会明显繁殖。各种炎症介质，如凝血因子、二十烷基类化合物、细胞因子、水解酶、活性氧和氮中间体，经常参与其中一个或两个过程。然而，如果读者接受我们的简化定义，那么本章所描述的原理是最容易理解的，即组织破坏性超敏反应过程杀死非激活的巨噬细胞，使结核杆菌在其中繁殖，细胞介导的免疫(CMI)过程使巨噬细胞的杀微菌能力强大到足以杀死或抑制分枝杆菌。巨噬细胞激活的免疫反应不能起作用，因为易感宿主只产生微弱的细胞免疫，在疾病的这个阶段，抵抗宿主的CMI还没有完全发育。人类的大多数肺结核感染在引起临床疾病之前就被控制住了。激活的巨噬细胞可以杀死它们摄取的结核杆菌。在正常情况下，即在感染开始之前，大多数肺泡巨噬细胞是非特异性激活的。为了治疗结核病并限制这种疾病向其他人传播，迫切需要防止液化或防止其继续存在的治疗剂。
Once the first small caseous tuberculous lesion is established, all subsequent battles occur in a host capable of both tissue damaging and macrophage-activating immune responses. Both tissue-damaging and macrophage-activating immune responses can stop the growth (i.e., multiplication) of tubercle bacilli, because these bacilli do not multiply appreciably in nonliquefied caseous necrotic tissue. Various inflammatory mediators, e.g., clotting factors, eicosanoids, cytokines, hydrolytic enzymes, and reactive oxygen and nitrogen intermediates, are frequently involved in one or both processes. However, the principles described in this chapter are most easily understood if the reader accepts our simplified definitions, namely, that the tissue-damaging hypersensitivity process kills nonactivated macrophages that have allowed tubercle bacilli to multiply within them and that the cell-mediated immunity (CMI) process makes the microbicidal power of macrophages strong enough to kill or inhibit mycobacteria. The macrophage-activating immune response could not be responsible, because the susceptible host develops only weak cell-mediated immunity, and at this stage of the disease, the CMI of the resistant host is not yet fully developed. The majority of pulmonary tuberculous infections of human beings are arrested before they cause clinical disease. Activated macrophages can kill the tubercle bacilli they ingest. Under normal conditions, i.e., before infection begins, most of the alveolar macrophages are nonspecifically activated. Therapeutic agents to prevent liquefaction or to prevent its continuation are greatly needed to treat tuberculosis and limit the spread of this disease to other people.
影响因子：
158.5
作者：
SELWYN, PA;HARTEL, D;FRIEDLAND, GH
通讯作者：
FRIEDLAND, GH