Ahmari Niousha, Hayward Linda F, Zubcevic Jasenka
Department of Physiology and Functional Genomics, College of Medicine, University of Florida, Gainesville, FL, USA.
Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL, USA.
Exp Physiol. 2020 Nov;105(11):1815-1826. doi: 10.1113/EP088247. Epub 2020 Sep 25.
What is the topic of this review? This manuscript provides a review of the current understanding of the role of the sympathetic nervous system in regulation of bone marrow-derived immune cells and the effect that the infiltrating bone marrow cells may have on perpetuation of the sympathetic over-activation in hypertension. What advances does it highlight? We highlight the recent advances in understanding of the neuroimmune interactions both peripherally and centrally as they relate to blood pressure control.
The sympathetic nervous system (SNS) plays a crucial role in maintaining physiological homeostasis, in part by regulating, integrating and orchestrating processes between many physiological systems, including the immune system. Sympathetic nerves innervate all primary and secondary immune organs, and all cells of the immune system express β-adrenoreceptors. In turn, immune cells can produce cytokines, chemokines and neurotransmitters capable of modulating neuronal activity and, ultimately, SNS activity. Thus, the essential role of the SNS in the regulation of innate and adaptive immune functions is mediated, in part, via β-adrenoreceptor-induced activation of bone marrow cells by noradrenaline. Interestingly, both central and systemic inflammation are well-established hallmarks of hypertension and its co-morbidities, including an inflammatory process involving the transmigration and infiltration of immune cells into tissues. We propose that physiological states that prolong β-adrenoreceptor activation in bone marrow can disrupt neuroimmune homeostasis and impair communication between the immune system and SNS, leading to immune dysregulation, which, in turn, is sustained via a central mechanism involving neuroinflammation.
本综述的主题是什么？本文对目前关于交感神经系统在调节骨髓源性免疫细胞中的作用以及浸润骨髓细胞可能对高血压中交感神经过度激活的持续存在产生的影响的理解进行了综述。它突出了哪些进展？我们突出了在理解外周和中枢神经免疫相互作用与血压控制之间关系方面的最新进展。
交感神经系统（SNS）在维持生理稳态中起着关键作用，部分是通过调节、整合和协调包括免疫系统在内的许多生理系统之间的过程。交感神经支配所有一级和二级免疫器官，免疫系统的所有细胞都表达β - 肾上腺素能受体。反过来，免疫细胞可以产生能够调节神经元活动并最终调节交感神经系统活动的细胞因子、趋化因子和神经递质。因此，交感神经系统在调节先天性和适应性免疫功能中的重要作用部分是通过β - 肾上腺素能受体诱导去甲肾上腺素激活骨髓细胞来介导的。有趣的是，中枢和全身性炎症都是高血压及其合并症的公认特征，包括涉及免疫细胞向组织迁移和浸润的炎症过程。我们提出，延长骨髓中β - 肾上腺素能受体激活的生理状态会破坏神经免疫稳态并损害免疫系统与交感神经系统之间的通讯，导致免疫失调，而免疫失调又通过涉及神经炎症的中枢机制得以维持。
