Role of the Immune system in chronic pain

Marchand, Fabien; Perretti, Mauro; McMahon, Stephen B.

doi:10.1038/nrn1700

Cited by 974 publications

(776 citation statements)

References 147 publications

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“…While the mechanisms underlying allodynia are still partially unknown, neuropathic hyperalgesia is associated with up-regulation of molecules, such as substance P and the excitatory neurotransmitter glutamate, which enhance the transmission of painful stimuli in DRG and spinal dorsal horn neurons (Fujita et al, 2007;Marchand et al, 2005;Ueda, 2006). Based on a review of studies published since 2000, it is estimated that 7% of the world's population is affected by NP (Andrew et al, 2014).…”

Section: Neuropathic Painmentioning

confidence: 99%

Lysophosphatidic acid receptors (LPARs): Potential targets for the treatment of neuropathic pain

2017

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Section: Neuropathic Painmentioning

confidence: 99%

Lysophosphatidic acid receptors (LPARs): Potential targets for the treatment of neuropathic pain

2017

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“…Chronic pain can be broadly categorized as chronic inflammatory pain and neuropathic pain. Chronic inflammatory pain arises as a consequence of inflammatory responses mounted by the immune system following tissue damage and generally abates after such damage is repaired [48,58]. Neuropathic pain, on the other hand, arises because of injury to a nerve caused by trauma, infection, or pathology, and is characterized by pain that persists long after the initiating event has healed [62,89].…”

Section: Introductionmentioning

confidence: 99%

P2X4 purinoceptor signaling in chronic pain

Trang

Salter

2012

Purinergic Signalling

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ATP, acting via P2 purinergic receptors, is a known mediator of inflammatory and neuropathic pain. There is increasing evidence that the ATP-gated P2X4 receptor (P2X4R) subtype is a locus through which activity of spinal microglia and peripheral macrophages instigate pain hypersensitivity caused by inflammation or by injury to a peripheral nerve. The present article highlights the recent advances in our understanding of microglia-neuron interactions in neuropathic pain by focusing on the signaling and regulation of the P2X4R. We will also develop a framework for understanding converging lines of evidence for involvement of P2X4Rs expressed on macrophages in peripheral inflammatory pain.

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“…Indeed in the past several years, more and more attention has been paid to neuron-glia interaction as a driving force for the development and maintenance of abnormal pain (reviewed in Ji & Strichartz, 2004;Marchand et al, 2005;Tsuda et al, 2005;Watkins et al, 2001). Glia activation in the spinal cord after nerve injury was first associated with pain behavior in 1991 (Garrison et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Do glial cells control pain?

Wen²,

et al. 2007

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Management of chronic pain is a real challenge, and current treatments focusing on blocking neurotransmission in the pain pathway have only resulted in limited success. Activation of glia cells has been widely implicated in neuroinflammation in the central nervous system, leading to neruodegeneration in many disease conditions such as Alzheimer's and multiple sclerosis. The inflammatory mediators released by activated glial cells, such as tumor necrosis factor-α and interleukin-1β can not only cause neurodegeneration in these disease conditions, but also cause abnormal pain by acting on spinal cord dorsal horn neurons in injury conditions. Pain can also be potentiated by growth factors such as BDNF and bFGF that are produced by glia to protect neurons. Thus, glia cells can powerfully control pain when they are activated to produce various pain mediators. We will review accumulating evidence supporting an important role of microglia cells in the spinal cord for pain control under injury conditions (e.g. nerve injury). We will also discuss possible signaling mechanisms in particular MAP kinase pathways that are critical for glia control of pain. Investigating signaling mechanisms in microglia may lead to more effective management of devastating chronic pain.

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Role of the Immune system in chronic pain

Cited by 974 publications

References 147 publications

Lysophosphatidic acid receptors (LPARs): Potential targets for the treatment of neuropathic pain

Lysophosphatidic acid receptors (LPARs): Potential targets for the treatment of neuropathic pain

P2X4 purinoceptor signaling in chronic pain

Do glial cells control pain?

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