Aim:Peripheral cytokines contribute to arthritis and bone cancer pain through sensory nerve actions.However,increased spinal cytokine and glial filament expression,coined neuroinflammation,has also been proposed to pl...Aim:Peripheral cytokines contribute to arthritis and bone cancer pain through sensory nerve actions.However,increased spinal cytokine and glial filament expression,coined neuroinflammation,has also been proposed to play a part in chronic pain.Therefore,spinal cord,dorsal root ganglia and circulating cytokines were compared in murine arthritis and bone cancer models in relationship to behavioral signs of pain.Methods:Exploratory behaviors were studied after intra-articular complete Freund’s adjuvant or bone intramedullary sarcoma cell injection.Nervous tissue and blood cytokine expression were determined by real-time polymerase chain reaction(PCR)and multiplex immunoassays,respectively.Results:PCR analysis did not reveal any hallmark of spinal neuroinflammation in spontaneously-behaving mice with cartilage or bone lesions.However,imposed paw stimulation during joint inflammation increased spinal interleukin-1β(IL-1β)expression.Spontaneous paw guarding during rearing was displayed by animals with joint inflammation and bone destruction and was accompanied by increased circulating IL-6 and monocyte chemoattractant protein-1,respectively.In addition,dorsal root ganglia were found to constitutively express receptors for this chemotactic cytokine.Conclusion:Our findings indicate that spinal neuroinflammation is not a necessary condition for chronic pain and suggest that circulating cytokine action in dorsal root ganglia may contribute to experimental joint inflammation and bone cancer pain.展开更多
文摘Aim:Peripheral cytokines contribute to arthritis and bone cancer pain through sensory nerve actions.However,increased spinal cytokine and glial filament expression,coined neuroinflammation,has also been proposed to play a part in chronic pain.Therefore,spinal cord,dorsal root ganglia and circulating cytokines were compared in murine arthritis and bone cancer models in relationship to behavioral signs of pain.Methods:Exploratory behaviors were studied after intra-articular complete Freund’s adjuvant or bone intramedullary sarcoma cell injection.Nervous tissue and blood cytokine expression were determined by real-time polymerase chain reaction(PCR)and multiplex immunoassays,respectively.Results:PCR analysis did not reveal any hallmark of spinal neuroinflammation in spontaneously-behaving mice with cartilage or bone lesions.However,imposed paw stimulation during joint inflammation increased spinal interleukin-1β(IL-1β)expression.Spontaneous paw guarding during rearing was displayed by animals with joint inflammation and bone destruction and was accompanied by increased circulating IL-6 and monocyte chemoattractant protein-1,respectively.In addition,dorsal root ganglia were found to constitutively express receptors for this chemotactic cytokine.Conclusion:Our findings indicate that spinal neuroinflammation is not a necessary condition for chronic pain and suggest that circulating cytokine action in dorsal root ganglia may contribute to experimental joint inflammation and bone cancer pain.
