Interactions between the immune and nervous systems in pain

By K. Ren, R. Dubner. Nature Medicine, 2010

791 citations recorded by the source corpus.

Immune cells and glia interact with neurons to alter pain sensitivity and to mediate the transition from acute to chronic pain. In response to injury, resident immune cells are activated and blood-borne immune cells are recruited to the site of injury. Immune cells not only contribute to immune protection but also initiate the sensitization of peripheral nociceptors. Through the synthesis and release of inflammatory mediators and interactions with neurotransmitters and their receptors, the immune cells, glia and neurons form an integrated network that coordinates immune responses and modulates the excitability of pain pathways. The immune system also reduces sensitization by producing immune-derived analgesic and anti-inflammatory or proresolution agents. A greater understanding of the role of the immune system in pain processing and modulation reveals potential targets for analgesic drug development and new therapeutic opportunities for managing chronic pain.

Subfields: Behavioral Neuroscience, Cellular and Molecular Neuroscience, Physiology

View Paper: https://www.semanticscholar.org/paper/dc235ccd74a7fca559875ae1477e8fe04a52da10

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Behavioral Neuroscience

1. Michael R. Irwin
2. George M. Slavich
3. Keith Bredemeier
4. A. Beck

In Cellular and Molecular Neuroscience

1. R. Ji
2. Michael R. Irwin
3. Maiken Nedergaard
4. George M. Slavich
5. M. Sofroniew
6. Clifford J. Woolf

In Physiology

1. T. Berta
2. Maiken Nedergaard
3. Michael R. Irwin
4. R. Ji
5. George M. Slavich
6. Clifford J. Woolf
7. Alban Latremoliere

Citations in the corpus

• Glia and pain: Is chronic pain a gliopathy? (2013, background): “Painful syndromes are associated with different glial activation states: (1) glial reaction (ie, upregulation of glial markers such as IBA1 and glial fibrillary acidic protein (GFAP) and/or morphological changes, including hypertrophy, proliferation, and modifications of glial networks); (2)…”
• From Stress to Inflammation and Major Depressive Disorder: A Social Signal Transduction Theory of Depression (2014, background): “In this context, it is notable that chronic pain has also been found to be highly comorbid with depression (Backonja, Coe, Muller, & Schell, 2008; Bair, Robinson, Katon, & Kroenke, 2003; Marchand, Perretti, & McMahon, 2005; Ren & Dubner, 2010; Samad et al., 2001).”
• Cytokines and Chemokines at the Crossroads of Neuroinflammation, Neurodegeneration, and Neuropathic Pain (2013, background): “This chemokine participates in the development of neuropathic pain through its receptors CCR1 and CCR5, which are located in Schwann cells and macrophages [239].”