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Monocytes expressing CX3CR1 orchestrate the development of vincristine-induced pain
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Monocytes expressing CX3CR1 orchestrate the development of vincristine-induced pain
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Journal Article
Monocytes expressing CX3CR1 orchestrate the development of vincristine-induced pain
2014
Overview
A major dose-limiting side effect associated with cancer-treating antineoplastic drugs is the development of neuropathic pain, which is not readily relieved by available analgesics. A better understanding of the mechanisms that underlie pain generation has potential to provide targets for prophylactic management of chemotherapy pain. Here, we delineate a pathway for pain that is induced by the chemotherapeutic drug vincristine sulfate (VCR). In a murine model of chemotherapy-induced allodynia, VCR treatment induced upregulation of endothelial cell adhesion properties, resulting in the infiltration of circulating CX3CR1⁺ monocytes into the sciatic nerve. At the endothelial-nerve interface, CX3CR1⁺ monocytes were activated by the chemokine CX3CL1 (also known as fractalkine [FKN]), which promoted production of reactive oxygen species that in turn activated the receptor TRPA1 in sensory neurons and evoked the pain response. Furthermore, mice lacking CX3CR1 exhibited a delay in the development of allodynia following VCR administration. Together, our data suggest that CX3CR1 antagonists and inhibition of FKN proteolytic shedding, possibly by targeting ADAM10/17 and/or cathepsin S, have potential as peripheral approaches for the prophylactic treatment of chemotherapy-induced pain.
Publisher
American Society for Clinical Investigation
Subject
/ Animals
/ Antineoplastic Agents, Phytogenic - adverse effects
/ Antineoplastic Agents, Phytogenic - pharmacology
/ Chemokine CX3CL1 - metabolism
/ Complications and side effects
/ Gene Expression Regulation - drug effects
/ Gene Expression Regulation - genetics
/ Hyperalgesia - chemically induced
/ Mice
/ Neurons
/ Pain
/ Receptors, Chemokine - genetics
/ Receptors, Chemokine - metabolism
