Division of Rheumatology, Geneva University Hospital, Geneva, Switzerland.
Curr Rheumatol Rep. 2010 Oct;12(5):370-8. doi: 10.1007/s11926-010-0124-z.
In inflammatory disorders such as rheumatoid arthritis, cytokines and danger signals are sensed by the central nervous system, which adapts behavior and physiologic responses during systemic stress. The central nervous system can also signal the periphery to modulate inflammation through efferent hormonal and neuronal pathways. The brain and spinal cord are involved in this bidirectional interaction. A variety of neuronal pathways that modulate synovial inflammation have been implicated, including the sympathetic and the parasympathetic branches of the autonomic system. Another mechanism, the dorsal root reflex, involves antidromic signaling along somatic afferent fibers that influences joint inflammation by releasing neuropeptides and other neuromediators in the periphery. Some of the neurotransmitters and neuroreceptors involved have been identified in preclinical models and represent novel targets for the treatment of rheumatic diseases.
在炎症性疾病(如类风湿关节炎)中,细胞因子和危险信号被中枢神经系统感知,中枢神经系统会在全身性应激期间调整行为和生理反应。中枢神经系统还可以通过传出激素和神经元途径向外周发出信号以调节炎症。大脑和脊髓参与这种双向相互作用。已经涉及到多种调节滑膜炎症的神经元途径,包括自主神经系统的交感和副交感分支。另一种机制是背根反射,涉及沿着躯体传入纤维的逆行信号,通过在外周释放神经肽和其他神经递质来影响关节炎症。一些已在临床前模型中确定的神经递质和神经受体代表了风湿性疾病治疗的新靶点。