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Involvement of inflammatory mediators in neuropathic pain caused by vincristine.
Int Rev Neurobiol. 2009; 85:179-90.IR

Abstract

Elucidation of the mechanism of neuropathic pain caused by vincristine is required because long-term treatment with this anticancer agent often causes neuropathic pain. We refer to the involvement of inflammatory mediators in vincristine-induced neuropathic pain in this review. Several reports using rodents have shown that long-lasting neuropathic pain (mechanical allodynia) is caused by repeated systemic injection of vincristine. Vincristine damaged Schwann cells and DRG neurons in this model. Vincristine-induced macrophage infiltration in the peripheral nervous system (PNS) and macrophage-derived IL-6 elicited mechanical allodynia. These findings proved that inhibition of IL-6 function prevented neuropathic pain caused by vincristine. In the central nervous system (CNS), activation of microglia and astrocytes in the spinal cord were demonstrated after long-term vincristine treatment. TNF-alpha was upregulated in activated microglia and astrocytes, and inhibition of TNF-alpha function attenuated neuropathic pain caused by vincristine. These results suggest that vincristine induces macrophage infiltration to the damaged PNS, and that macrophage-derived inflammatory cytokines such as IL-6 elicits neuroinflammation. Signal transduction of pain from the PNS to the CNS activates microglia and astrocytes, and these activated glial cells release inflammatory cytokines such as TNF-alpha. In the CNS, these inflammatory cytokines have an important role in the neuropathic pain caused by vincristine. Immune-modulating agents that prevent activation of immune cells and/or the inhibitory agents of inflammatory cytokines could prevent the neuropathic pain caused by vincristine. These agents could increase the tolerability of vincristine when used for the treatment of leukemia and lymphoma.

Authors+Show Affiliations

Department of Pharmacology, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-0012, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

19607970

Citation

Kiguchi, Norikazu, et al. "Involvement of Inflammatory Mediators in Neuropathic Pain Caused By Vincristine." International Review of Neurobiology, vol. 85, 2009, pp. 179-90.
Kiguchi N, Maeda T, Kobayashi Y, et al. Involvement of inflammatory mediators in neuropathic pain caused by vincristine. Int Rev Neurobiol. 2009;85:179-90.
Kiguchi, N., Maeda, T., Kobayashi, Y., Saika, F., & Kishioka, S. (2009). Involvement of inflammatory mediators in neuropathic pain caused by vincristine. International Review of Neurobiology, 85, 179-90. https://doi.org/10.1016/S0074-7742(09)85014-9
Kiguchi N, et al. Involvement of Inflammatory Mediators in Neuropathic Pain Caused By Vincristine. Int Rev Neurobiol. 2009;85:179-90. PubMed PMID: 19607970.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of inflammatory mediators in neuropathic pain caused by vincristine. AU - Kiguchi,Norikazu, AU - Maeda,Takehiko, AU - Kobayashi,Yuka, AU - Saika,Fumihiro, AU - Kishioka,Shiroh, PY - 2009/7/18/entrez PY - 2009/7/18/pubmed PY - 2009/9/11/medline SP - 179 EP - 90 JF - International review of neurobiology JO - Int Rev Neurobiol VL - 85 N2 - Elucidation of the mechanism of neuropathic pain caused by vincristine is required because long-term treatment with this anticancer agent often causes neuropathic pain. We refer to the involvement of inflammatory mediators in vincristine-induced neuropathic pain in this review. Several reports using rodents have shown that long-lasting neuropathic pain (mechanical allodynia) is caused by repeated systemic injection of vincristine. Vincristine damaged Schwann cells and DRG neurons in this model. Vincristine-induced macrophage infiltration in the peripheral nervous system (PNS) and macrophage-derived IL-6 elicited mechanical allodynia. These findings proved that inhibition of IL-6 function prevented neuropathic pain caused by vincristine. In the central nervous system (CNS), activation of microglia and astrocytes in the spinal cord were demonstrated after long-term vincristine treatment. TNF-alpha was upregulated in activated microglia and astrocytes, and inhibition of TNF-alpha function attenuated neuropathic pain caused by vincristine. These results suggest that vincristine induces macrophage infiltration to the damaged PNS, and that macrophage-derived inflammatory cytokines such as IL-6 elicits neuroinflammation. Signal transduction of pain from the PNS to the CNS activates microglia and astrocytes, and these activated glial cells release inflammatory cytokines such as TNF-alpha. In the CNS, these inflammatory cytokines have an important role in the neuropathic pain caused by vincristine. Immune-modulating agents that prevent activation of immune cells and/or the inhibitory agents of inflammatory cytokines could prevent the neuropathic pain caused by vincristine. These agents could increase the tolerability of vincristine when used for the treatment of leukemia and lymphoma. SN - 0074-7742 UR - https://www.unboundmedicine.com/medline/citation/19607970/Involvement_of_inflammatory_mediators_in_neuropathic_pain_caused_by_vincristine_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0074-7742(09)85014-9 DB - PRIME DP - Unbound Medicine ER -