Background:
Some of the current challenges and complications of cancer therapy are chemotherapy-
induced peripheral neuropathy (CIPN) and the neuropathic pain that are associated with
this condition. Many major chemotherapeutic agents can cause neurotoxicity, significantly modulate
the immune system and are always accompanied by various adverse effects. Recent evidence suggests
that cross-talk occurs between the nervous system and the immune system during treatment with chemotherapeutic
agents; thus, an emerging concept is that neuroinflammation is one of the major
mechanisms underlying CIPN, as demonstrated by the upregulation of chemokines. Chemokines were
originally identified as regulators of peripheral immune cell trafficking, and chemokines are also expressed
on neurons and glial cells in the central nervous system.
Objective:
In this review, we collected evidence demonstrating that chemokines are potential mediators
and contributors to pain signalling in CIPN. The expression of chemokines and their receptors,
such as CX3CL1/CX3CR1, CCL2/CCR2, CXCL1/CXCR2, CXCL12/CXCR4 and CCL3/CCR5, is
altered in the pathological conditions of CIPN, and chemokine receptor antagonists attenuate neuropathic
pain behaviour.
Conclusion:
By understanding the mechanisms of chemokine-mediated communication, we may reveal
chemokine targets that can be used as novel therapeutic strategies for the treatment of CIPN.
Behavioral, Electrophysiological, and Histological Characterization of a New Rat Model for Neoadjuvant Chemotherapy–Induced Neuropathic Pain: Therapeutic Potential of Duloxetine and Allopregnanolone Concomitant Treatment
