Neurogenic Regulation of Bradykinin-Induced Synovitis

Add time:08/29/2019    Source:sciencedirect.com

Substantial evidence is described supporting the hypothesis that bradykinin-induced synovial inflammation is dependent on the sympathetic postganglionic neuron. In addition, experimental data indicate that a sympathetic–C-fiber afferent neuron integration plays a role in acute and chronic inflammation in the synovium and other tissues. For example, sympathetic–C-fiber coupling takes place during the skin inflammatory response [146,212,213]. Specifically, sympathetic efferent activity acts on peripheral adrenergic receptors to enhance C-fiber sensitization, thereby augmenting the generation of dorsal root reflexes that produce vasodilatation. However, to firmly establish such integration in synovial tissue, further studies are needed that employ controlled selective activation of the afferents supplying the synovium, e.g., by electrical stimulation of the corresponding dorsal roots [211].Furthermore, the evidence suggests that there exists a functionally distinct sympathetic efferent pathway that enables the central nervous system to modulate the inflammatory response by acting on components of the immune system [103,116]. Specifically, at a systemic level activity in the sympathetic neurons modulates immune cell function via innervation of lymphoid organs and by direct contact with lymphocytes and macrophages [214], and at the local level the sympathetic modulates the sensitivity of nociceptors, directly or via immune cells and their signaling molecules (e.g., cytokines). A schematic representation of the interaction of some key systems in the control of synovial inflammation is shown in Fig. 4.

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