Neural-immune interactions in dorsal root ganglia

Abstract

Interleukin-1 (IL-1) β is a proinflammatory cytokine that is produced by a large variety of cells, including macrophages, fibroblasts, mesangial cells and endothelial cells, and is believed to play important roles in the inflammatory responses, including hyperalgesia. Hyperalgesia is characterized by intensified pain with a reduced threshold to somatic stimulation, and it is involved in chronic inflammatory disease. Substance P (SP), an undecapeptide, has been shown to relay noxious signals as a neurotransmitter in primary afferent neurons. Thus it is expected that the change of neuropeptide activities in primary afferent neurons is attributed to inflammatory hyperalgesia by IL-1β. In our recent studies, IL-1β was found to stimulate SP release from cultured dorsal root ganglion cells via the cyclooxygenase system. These studies provide a new insight in the neural-immune intercommunication involved in the pain-regulation system observed in inflammation-induced hyperalgesia.