Dr. Roland Staud
The nervous system as well as the immune system use common signaling molecules for intra- and inter-system communications. Specifically, both entities produce a similar array of peptide and non-peptide transmitters that act on a common set of receptors present in the two systems. One important set of such signaling molecules are cytokines. The wide distribution of cytokine receptors throughout the body, including the immune and the nervous system allows direct communication between these two entities. In addition to cytokines the nervous system and immune system also communicate with each other using shared ligands such as neurotransmitters and neuroendocrine hormones, and their respective receptors. Some of the most important clinical interactions between these two systems are associated with the “sickness response” as well as pain and analgesia. This “sickness response” which has been frequently attributed to inflammatory cytokines, strongly resembles the core symptoms of fibromyalgia and other Central Sensitivity Syndromes (CSS). Therefore a large number of research studies have focused on the relationship between peripheral cytokines and CSS. However, a lack of consistent associations was observed between CSS symptoms and peripheral cytokines which seem to suggest that maybe cytokines abnormalities of the central nervous system contribute to the pathogenesis of these illnesses. Better knowledge of cytokine -nervous system interactions may ultimately benefit the development of interventions that improve CSS manifestations including the “sickness response” and chronic pain.
細胞因子的接受體遍布全身，使得神經系統與免疫系統可以直接聯繫。除了細胞因子(cytokines )外，神經系統與免疫系統的聯繫，還有他們共享的配體(ligand)；例如神經傳導素，神經內分泌荷爾蒙，和他們專屬的接受體。因此，神經系統與免疫系統互相作用，在臨床表現出「生病反應sickness response」，異痛症或痛覚異常。這種「生病反應」，就像纖維肌痛症，和其他中樞敏感症(CSS )的主要症狀。歸因於細胞因子作怪。因此，很多研究的焦點，都放在周邊細胞因子和中樞敏感症之間的關係。然而，研究卻發現兩者之間卻沒有 一致的關聯，這意味著：中樞神經系統細胞因子的失常，可能是造成疾病的原因，而非周邊細胞因子。越來越多有関細胞因子與神經系統交互作用的知識，將有利改善纖維肌痛症和中樞敏感症產生的「病態反應」和慢性疼痛。