Abstract
The development of new therapeutic approaches to the treatment of painful neuropathies requires a better understanding of the mechanisms that underlie chronic pain syndromes. There is increasing evidence that immune competent cells such as microglia contribute to the development of chronic pain states. Chemokines play a pivotal role in mediating neuronal-microglial communication which leads to increased nociception. Fractalkine (FKN) is structurally unique amongst the family of chemokines and their receptors and expressed both in the central nervous system and peripheral nerves, as well as in endothelial cells and lymphocytes. Signalling via the CX3CR1 receptor, FKN is able to mediate critical physiological functions necessary for immune regulation. In its soluble forms FKN mediates chemotaxis of immune cells whilst membrane bound FKN acts as an adhesion molecule mediating leukocyte capture and infiltration. As FKN/CX3CR1 is such a key signalling pair for homeostatic functions it is not surprising that it is implicated in a large number of diseases in which imbalance of the immune system is implied. Here we review the evidence that FKN/CX3CR1 mediates neuron-microglial communication in chronic pain states and is therefore key in the development of neuropathic pain. In addition, the contribution of FKN/CX3CR1 signalling to the pathogenesis and progression of two chronic inflammatory conditions, atherosclerosis and rheumatoid arthritis, are discussed.
Keywords: Fractalkine/CX3CR1, chronic pain, atherosclerosis, immune competent cells, microglia, Chemokines, neuronal-microglial communication, nociception, Fractalkine, CX3CR1 receptor, immune regulation, FKN/CX3CR1, chronic inflammatory conditions, rheumatoid arthritis
Current Pharmaceutical Biotechnology
Title: Fractalkine/CX3CR1 Signalling in Chronic Pain and Inflammation
Volume: 12 Issue: 10
Author(s): Anna K. Clark, Amelia A. Staniland and Marzia Malcangio
Affiliation:
Keywords: Fractalkine/CX3CR1, chronic pain, atherosclerosis, immune competent cells, microglia, Chemokines, neuronal-microglial communication, nociception, Fractalkine, CX3CR1 receptor, immune regulation, FKN/CX3CR1, chronic inflammatory conditions, rheumatoid arthritis
Abstract: The development of new therapeutic approaches to the treatment of painful neuropathies requires a better understanding of the mechanisms that underlie chronic pain syndromes. There is increasing evidence that immune competent cells such as microglia contribute to the development of chronic pain states. Chemokines play a pivotal role in mediating neuronal-microglial communication which leads to increased nociception. Fractalkine (FKN) is structurally unique amongst the family of chemokines and their receptors and expressed both in the central nervous system and peripheral nerves, as well as in endothelial cells and lymphocytes. Signalling via the CX3CR1 receptor, FKN is able to mediate critical physiological functions necessary for immune regulation. In its soluble forms FKN mediates chemotaxis of immune cells whilst membrane bound FKN acts as an adhesion molecule mediating leukocyte capture and infiltration. As FKN/CX3CR1 is such a key signalling pair for homeostatic functions it is not surprising that it is implicated in a large number of diseases in which imbalance of the immune system is implied. Here we review the evidence that FKN/CX3CR1 mediates neuron-microglial communication in chronic pain states and is therefore key in the development of neuropathic pain. In addition, the contribution of FKN/CX3CR1 signalling to the pathogenesis and progression of two chronic inflammatory conditions, atherosclerosis and rheumatoid arthritis, are discussed.
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Cite this article as:
K. Clark Anna, A. Staniland Amelia and Malcangio Marzia, Fractalkine/CX3CR1 Signalling in Chronic Pain and Inflammation, Current Pharmaceutical Biotechnology 2011; 12 (10) . https://dx.doi.org/10.2174/138920111798357465
DOI https://dx.doi.org/10.2174/138920111798357465 |
Print ISSN 1389-2010 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4316 |
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