Immune-mediated processes implicated in chemotherapy-induced peripheral neuropathy. (March 2017)

• Record Type: Journal Article
• Authors: Lees, Justin G.; Makker, Preet G.S.; Tonkin, Ryan S.; Abdulla, Munawwar; Park, Susanna B.; Goldstein, David; Moalem-Taylor, Gila
• Is Part Of: European journal of cancer. Volume 73(2017)
• Page Start: 22
• Page End: 29
• Publication Date: 2017-03
• Subjects: Chemotherapy-induced peripheral neuropathy -- Neurotoxicity -- Neuroinflammation -- Immune cell activation -- Hypersensitivity -- Paraesthesia; Cancer -- Periodicals; Neoplasms -- Periodicals; Cancer -- Périodiques; Cancer; Tumors; Electronic journals; Periodicals; Electronic journals; 616.994
• DOI: 10.1016/j.ejca.2016.12.006
• Languages: English
• ISSNs: 0959-8049

Abstract

Abstract: Chemotherapy-induced peripheral neuropathy (CIPN) and associated neuropathic pain are challenging complications of cancer treatment. Many of the major classes of chemotherapeutics can cause neurotoxicity and significantly modulate the immune system. There is ongoing investigation regarding whether reciprocal crosstalk between the nervous and immune systems occurs and, indeed, contributes to neuropathic pain during treatment with chemotherapeutics. An emerging concept is that neuroinflammation is one of the major mechanisms underlying CIPN. Here, we discuss recent findings, which provide insight into this complex process of neuroimmune interactions. Findings show limited infiltration of leukocytes into the nervous system of CIPN animals and varying degrees of peripheral and central glial activation depending on the chemotherapeutic drug, dose, schedule, and timing. Most evidence suggests an increase in pro-inflammatory cytokine expression and changes in immune signalling pathways. There is, however, limited evidence available from human studies and it remains unclear whether neuroinflammatory responses are the cause of neuropathy or a bystander effect of the chemotherapy treatment. Highlights: Chemotherapy-induced peripheral neuropathy (CIPN) is an increasingly problematic issue with no acceptable treatment option. An emerging concept is that neuroimmune responses are a primary cause of CIPN. CIPN models demonstrate varied peripheral and central glial activation and increased pro-inflammatory cytokine expression. Few clinical studies have investigated the neuroimmune response associated with CIPN.