Stress-evoked sterile inflammation, danger associated molecular patterns (DAMPs), microbial associated molecular patterns (MAMPs) and the inflammasome
Stress-evoked sterile inflammation, danger associated molecular patterns (DAMPs), microbial associated molecular patterns (MAMPs) and the inflammasome
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DOI：
10.1016/j.bbi.2012.08.012
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发表时间：
2013-01-01
影响因子：
15.1
通讯作者：
Fleshner, Monika
中科院分区：
文献类型：
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作者：
Fleshner, Monika
自心理神经免疫学研究领域成立以来，人们一直认为对压力源的生理反应包括免疫功能的调节。研究人员最初专注于应激对细胞迁移和免疫抑制的影响，以及由此导致的肿瘤监视，抗病毒T细胞免疫和抗原特异性抗体应答的减少。最近，人们已经清楚地认识到，暴露于压力源也会增强先天免疫过程。例如，应激源暴露可以改变骨髓谱系细胞如单核细胞、巨噬细胞、嗜中性粒细胞和小胶质细胞的活化状态，导致致敏状态。此外，应激暴露增加了血液和组织中大量炎症蛋白的合成和释放（即，脾、肝、脂肪、脉管系统和脑）。应激诱发的先天免疫“唤醒”的机制仍然未知。本次总统演讲的目标如下：（1）提供一个个性化的，简要概述的压力和免疫力，重点是“唤醒”先天免疫;（2）描述无菌炎症过程和炎症体的作用;和（3）表明这些相同的过程可能有助于引发骨髓细胞和炎症蛋白反应（全身和组织）在没有病原体的情况下由应激产生。(C)2012 Elsevier Inc. All rights reserved.
Since the inception of the field of psychoneuroimmunolology research, there has been an appreciation that the physiological response to stressors includes modulation of immune function. Investigators initially focused on the effect of stress on cellular migration and immunosuppression and the resultant decreases in tumor surveillance, anti-viral T cell immunity and antigen-specific antibody responses. More recently, it has become clear that exposure to stressors also potentiate innate immune processes. Stressor exposure, for example, can change the activation status of myeloid lineage cells such as monocytes, macrophages, neutrophils, and microglia, leading to a primed state. In addition, stressor exposure increases the synthesis and release of a vast cadre' of inflammatory proteins both in the blood and within tissues (i.e., spleen, liver, adipose, vasculature and brain). The mechanisms for stress-evoked innate immune 'arousal' remain unknown. The goals of this presidential address are the following: (1) offer a personalized, brief overview of stress and immunity with a focus on 'aroused' innate immunity; (2) describe sterile inflammatory processes and the role of the inflammasome; and (3) suggest that these same processes likely contribute to primed myeloid cells and inflammatory protein responses (systemic and tissue) produced by stress in the absence of pathogens. (C) 2012 Elsevier Inc. All rights reserved.