Increased circulating rather than spinal cytokines accompany chronic pain behaviors in experimental bone cancer and arthritis

发表时间：2015-11-18 浏览次数：1751次

引用：

Pourtau L, Heeringa AN, Rovere C, Aubert A, Nahon JL, Miraux S, Konsman JP. Incr

关键词：

作者：

Line Pourtau1, Amarins Nieske Heeringa1, Carole Ro

作者单位：

1 CNRS, PsychoNeuroImmunologie, Nutrition et Génét

出版年份：

2014

期刊页数：

153-160

收录者：

其他外文数据库

摘要：

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.

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