Lee Jinhee, Hartman Michelle, Kornfeld Hardy
Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA.
Yonsei Med J. 2009 Feb 28;50(1):1-11. doi: 10.3349/ymj.2009.50.1.1. Epub 2009 Feb 24.
Mycobacterium tuberculosis (Mtb) is an intracellular pathogen that infects alveolar macrophages following aerosol transmission. Lung macrophages provide a critical intracellular niche that is required for Mtb to establish infection in the human host. This parasitic relationship is made possible by the capacity of Mtb to block phagosome maturation following entry into the host macrophage, creating an environment that supports bacillary replication. Apoptosis is increasingly understood to play a role in host defense against intracellular pathogens including viruses, fungi, protozoa and bacteria. In the last 15 years an understanding of the role that macrophage apoptosis plays in TB has begun to emerge. Here we review the history and current state of the art of this topic and we offer a model of the macrophage-pathogen interaction that takes into the account the complexities of programmed cell death and the relationship between various death signaling pathways and host defense in TB.
结核分枝杆菌(Mtb)是一种细胞内病原体,通过气溶胶传播感染肺泡巨噬细胞。肺巨噬细胞提供了一个关键的细胞内微环境,Mtb在人类宿主中建立感染需要该环境。Mtb进入宿主巨噬细胞后能够阻断吞噬体成熟,从而创造出一个支持细菌复制的环境,使得这种寄生关系成为可能。人们越来越认识到细胞凋亡在宿主抵御包括病毒、真菌、原生动物和细菌在内的细胞内病原体中发挥作用。在过去15年里,对巨噬细胞凋亡在结核病中所起作用的认识已开始显现。在此,我们回顾该主题的历史和当前技术水平,并提供一个巨噬细胞与病原体相互作用的模型,该模型考虑了程序性细胞死亡的复杂性以及结核病中各种死亡信号通路与宿主防御之间的关系。