The role of the macrophage in lung disease mediated by bacteria
The role of the macrophage in lung disease mediated by bacteria
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DOI：
10.1080/01902140701756562
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发表时间：
2007-12-01
影响因子：
1.7
通讯作者：
Dockrell, David H.
中科院分区：
文献类型：
--
作者：
Marriott, Helen M.;Dockrell, David H.
呼吸道感染是人类发病的主要原因，也是主要的死亡原因。下呼吸道是一个无菌的环境，宿主防御系统很好地清除细菌。这种反应既包括数字因素，也包括驻留和招募的细胞。肺泡巨噬细胞是弧形的组成部分，具有延年益寿的功能。在低剂量攻击后，肺泡巨噬细胞采用一套重叠的杀菌策略清除肺内的细菌。在较高剂量时，肺泡巨噬细胞的吞噬能力被压倒，但肺泡巨噬细胞帮助协调炎症反应。在感染的解决阶段。肺泡巨噬细胞参与了细胞的凋亡诱导和清除。这一过程下调了促炎细胞因子的产生。巨噬细胞的功能是通过诱导细胞凋亡来控制的。延迟性巨噬细胞凋亡有助于细菌清除和炎症反应的消退。MCL-1是一种半衰期很短的抗凋亡蛋白，是巨噬细胞存活的调节器，因此是宿主对肺部常见细菌病原体的反应的调节器。对肺炎链球菌和其他呼吸道细菌的研究进行了讨论，以阐明这些观点，并认为巨噬细胞凋亡的时间对于确定其对宿主病原体相互作用的整体影响是重要的。
Respiratory infections area major cause of human morbidity and a leading cause of death. The lower respiratory tract is a sterile environment and host defense is well developed to clear bacteria. This response includes both Numeral factors and resident and recruited cells. The alveolar macrophage is arc integral component and its long-lifespan aids function. Following low-dose challenge alveolar macrophages clear bacteria from the lung employing an over-lapping set of microbicidal strategies. At a higher-dose the phagocytic capacity of alveolar macrophages is overwhelmed but alveolar macrophages help orchestrate the inflammatory response. In the resolution phase of infection. alveolar macrophages contribute to apoptosis induction sand clearance of recruited cells. This process down-regulates pro-inflammatory cytokine production. Macrophage function is controlled by induction of apoplosis. Delayed-onset macrophage apoptosis contributes both to bacterial clearance and to resolution of the inflammatory response. Mcl-1, an anti-apoptotic protein with a very short half-life, is a hey regulator of macrophage survival and therefore of host responses to common bacterial pathogens in the lung. Studies involving Streptococcus pneumoniae and other respiratory bacteria are discussed to illustrate these points and ephasise that the timing of macrophage apoptosis is important in determining its overall effect on the host pathogen interaction.