A novel interaction between CX₃CR₁ and CCR₂ signalling in monocytes constitutes an underlying mechanism for persistent vincristine-induced pain.

ABSTRACT:

Background

A dose-limiting side effect of chemotherapeutic agents such as vincristine (VCR) is neuropathic pain, which is poorly managed at present. Chemokine-mediated immune cell/neuron communication in preclinical VCR-induced pain forms an intriguing basis for the development of analgesics. In a murine VCR model, CX₃CR₁ receptor-mediated signalling in monocytes/macrophages in the sciatic nerve orchestrates the development of mechanical hypersensitivity (allodynia). CX₃CR₁-deficient mice however still develop allodynia, albeit delayed; thus, additional underlying mechanisms emerge as VCR accumulates. Whilst both patrolling and inflammatory monocytes express CX₃CR₁, only inflammatory monocytes express CCR₂

SUBMITTER: Montague K 

PROVIDER: S-EPMC5889528 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature