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Diverse roles of endoplasmic reticulum stress sensors in bacterial infection
Molecular and Cellular Pediatrics Pub Date : 2016-02-16 , DOI: 10.1186/s40348-016-0037-7 Helena Pillich 1 , Maria Loose 1 , Klaus-Peter Zimmer 2 , Trinad Chakraborty 1
Molecular and Cellular Pediatrics Pub Date : 2016-02-16 , DOI: 10.1186/s40348-016-0037-7 Helena Pillich 1 , Maria Loose 1 , Klaus-Peter Zimmer 2 , Trinad Chakraborty 1
Affiliation
Bacterial infection often leads to cellular damage, primarily marked by loss of cellular integrity and cell death. However, in recent years, it is being increasingly recognized that, in individual cells, there are graded responses collectively termed cell-autonomous defense mechanisms that induce cellular processes designed to limit cell damage, enable repair, and eliminate bacteria. Many of these responses are triggered not by detection of a particular bacterial effector or ligand but rather by their effects on key cellular processes and changes in homeostasis induced by microbial effectors when recognized. These in turn lead to a decrease in essential cellular functions such as protein translation or mitochondrial respiration and the induction of innate immune responses that may be specific to the cellular deficit induced. These processes are often associated with specific cell compartments, e.g., the endoplasmic reticulum (ER). Under non-infection conditions, these systems are generally involved in sensing cellular stress and in inducing and orchestrating the subsequent cellular response. Thus, perturbations of ER homeostasis result in accumulation of unfolded proteins which are detected by ER stress sensors in order to restore the normal condition. The ER is also important during bacterial infection, and bacterial effectors that activate the ER stress sensors have been discovered. Increasing evidence now indicate that bacteria have evolved strategies to differentially activate different arms of ER stress sensors resulting in specific host cell response. In this review, we will describe the mechanisms used by bacteria to activate the ER stress sensors and discuss their role during infection.
中文翻译:
内质网应激传感器在细菌感染中的多种作用
细菌感染通常会导致细胞损伤,主要表现为细胞完整性丧失和细胞死亡。然而,近年来,人们越来越认识到,在单个细胞中,存在统称为细胞自主防御机制的分级反应,这些反应诱导旨在限制细胞损伤、修复和消除细菌的细胞过程。许多这些反应不是通过检测特定的细菌效应子或配体而触发的,而是通过它们对关键细胞过程的影响以及微生物效应子在被识别时诱导的体内平衡变化而触发的。这些反过来导致基本细胞功能的减少,例如蛋白质翻译或线粒体呼吸,以及可能对诱导的细胞缺陷具有特异性的先天免疫反应的诱导。这些过程通常与特定的细胞区室有关,例如内质网 (ER)。在非感染条件下,这些系统通常参与感知细胞压力以及诱导和协调随后的细胞反应。因此,内质网稳态的扰动导致内质网应激传感器检测到的未折叠蛋白的积累,以恢复正常状态。内质网在细菌感染期间也很重要,并且已经发现了激活内质网应激传感器的细菌效应物。现在越来越多的证据表明,细菌已经进化出策略来差异激活内质网应激传感器的不同臂,从而导致特定的宿主细胞反应。在这次审查中,
更新日期:2016-02-16
中文翻译:
内质网应激传感器在细菌感染中的多种作用
细菌感染通常会导致细胞损伤,主要表现为细胞完整性丧失和细胞死亡。然而,近年来,人们越来越认识到,在单个细胞中,存在统称为细胞自主防御机制的分级反应,这些反应诱导旨在限制细胞损伤、修复和消除细菌的细胞过程。许多这些反应不是通过检测特定的细菌效应子或配体而触发的,而是通过它们对关键细胞过程的影响以及微生物效应子在被识别时诱导的体内平衡变化而触发的。这些反过来导致基本细胞功能的减少,例如蛋白质翻译或线粒体呼吸,以及可能对诱导的细胞缺陷具有特异性的先天免疫反应的诱导。这些过程通常与特定的细胞区室有关,例如内质网 (ER)。在非感染条件下,这些系统通常参与感知细胞压力以及诱导和协调随后的细胞反应。因此,内质网稳态的扰动导致内质网应激传感器检测到的未折叠蛋白的积累,以恢复正常状态。内质网在细菌感染期间也很重要,并且已经发现了激活内质网应激传感器的细菌效应物。现在越来越多的证据表明,细菌已经进化出策略来差异激活内质网应激传感器的不同臂,从而导致特定的宿主细胞反应。在这次审查中,