Department of Microbiology and Immunology , University of Texas Medical Branch, 301 University Blvd, Galveston, Texas 77555 USA.
Department of Pathology, University of Texas Medical Branch , University of Texas Medical Branch, 301 University Blvd, Galveston, Texas 77555 USA.
Pathog Dis. 2020 Feb 1;78(1). doi: 10.1093/femspd/ftaa009.
Macrophages play an integral role in host defenses against intracellular bacterial pathogens. A remarkable plasticity allows for adaptation to the needs of the host to orchestrate versatile innate immune responses to a variety of microbial threats. Several bacterial pathogens have adapted to macrophage plasticity and modulate the classical (M1) or alternative (M2) activation bias towards a polarization state that increases fitness for intracellular survival. Here, we summarize the current understanding of the host macrophage and intracellular bacterial interface; highlighting the roles of M1/M2 polarization in host defense and the mechanisms employed by several important intracellular pathogens to modulate macrophage polarization to favor persistence or proliferation. Understanding macrophage polarization in the context of disease caused by different bacterial pathogens is important for the identification of targets for therapeutic intervention.
巨噬细胞在宿主防御细胞内细菌病原体中起着不可或缺的作用。其显著的可塑性使其能够适应宿主的需求，从而协调针对各种微生物威胁的多样先天免疫反应。几种细菌病原体已经适应了巨噬细胞的可塑性，并调节经典（M1）或替代（M2）激活偏向极化状态，从而提高细胞内生存能力。在这里，我们总结了宿主巨噬细胞和细胞内细菌界面的当前认识；强调了 M1/M2 极化在宿主防御中的作用，以及几种重要细胞内病原体用来调节巨噬细胞极化以促进存活或增殖的机制。了解不同细菌病原体引起的疾病中的巨噬细胞极化对于确定治疗干预的靶点非常重要。
