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The critical role of invading peripheral macrophage-derived interleukin-6 in vincristine-induced mechanical allodynia in mice.
Eur J Pharmacol. 2008 Sep 11; 592(1-3):87-92.EJ

Abstract

Although the clinical use of vincristine is limited by its adverse effect, neuropathic pain, the mechanism of this effect is poorly understood. Recently, reports demonstrated that inflammatory and immune responses play an important role in the neuropathic pain that follows peripheral nerve injury. In this study, we examined the role of macrophage-derived interleukin (IL)-6 in vincristine-induced mechanical allodynia. Vincristine sulfate (0.01-0.1 mg/kg, i.p.) was administered to male ICR mice and BALB/c mice once per day for 7 or 14 days. Mechanical allodynia was evaluated by withdrawal responses, using von Frey filaments from day 0 to day 28. In both ICR mice and BALB/c mice, significant dose-dependent increases in the percentage of withdrawal responses were observed from day 3 to day 28 following repeated administration of vincristine (0.1 mg/kg). As determined by immunohistochemistry, the number of macrophages in the region of the sciatic nerve and lumbar dorsal root ganglion was significantly increased on day 7 of vincristine administration. The expression of IL-6 was increased by vincristine administration and was co-localized in the invading macrophage. Moreover, a neutralizing antibody of IL-6, which was injected into areas surrounding the sciatic nerve on day 0, 3, and 6, significantly attenuated vincristine-induced mechanical allodynia from day 7 to day 28. In addition, the incidence of vincristine-induced mechanical allodynia in IL-6 knockout mice was lower than that in wild type mice from day 3 to day 28. These results suggest that the invading peripheral macrophage-derived IL-6 plays a critical role in vincristine-induced mechanical allodynia.

Authors+Show Affiliations

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

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18652822

Citation

Kiguchi, Norikazu, et al. "The Critical Role of Invading Peripheral Macrophage-derived Interleukin-6 in Vincristine-induced Mechanical Allodynia in Mice." European Journal of Pharmacology, vol. 592, no. 1-3, 2008, pp. 87-92.
Kiguchi N, Maeda T, Kobayashi Y, et al. The critical role of invading peripheral macrophage-derived interleukin-6 in vincristine-induced mechanical allodynia in mice. Eur J Pharmacol. 2008;592(1-3):87-92.
Kiguchi, N., Maeda, T., Kobayashi, Y., Kondo, T., Ozaki, M., & Kishioka, S. (2008). The critical role of invading peripheral macrophage-derived interleukin-6 in vincristine-induced mechanical allodynia in mice. European Journal of Pharmacology, 592(1-3), 87-92. https://doi.org/10.1016/j.ejphar.2008.07.008
Kiguchi N, et al. The Critical Role of Invading Peripheral Macrophage-derived Interleukin-6 in Vincristine-induced Mechanical Allodynia in Mice. Eur J Pharmacol. 2008 Sep 11;592(1-3):87-92. PubMed PMID: 18652822.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The critical role of invading peripheral macrophage-derived interleukin-6 in vincristine-induced mechanical allodynia in mice. AU - Kiguchi,Norikazu, AU - Maeda,Takehiko, AU - Kobayashi,Yuka, AU - Kondo,Toshikazu, AU - Ozaki,Masanobu, AU - Kishioka,Shiroh, Y1 - 2008/07/10/ PY - 2008/05/12/received PY - 2008/06/25/revised PY - 2008/07/05/accepted PY - 2008/7/26/pubmed PY - 2008/10/25/medline PY - 2008/7/26/entrez SP - 87 EP - 92 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 592 IS - 1-3 N2 - Although the clinical use of vincristine is limited by its adverse effect, neuropathic pain, the mechanism of this effect is poorly understood. Recently, reports demonstrated that inflammatory and immune responses play an important role in the neuropathic pain that follows peripheral nerve injury. In this study, we examined the role of macrophage-derived interleukin (IL)-6 in vincristine-induced mechanical allodynia. Vincristine sulfate (0.01-0.1 mg/kg, i.p.) was administered to male ICR mice and BALB/c mice once per day for 7 or 14 days. Mechanical allodynia was evaluated by withdrawal responses, using von Frey filaments from day 0 to day 28. In both ICR mice and BALB/c mice, significant dose-dependent increases in the percentage of withdrawal responses were observed from day 3 to day 28 following repeated administration of vincristine (0.1 mg/kg). As determined by immunohistochemistry, the number of macrophages in the region of the sciatic nerve and lumbar dorsal root ganglion was significantly increased on day 7 of vincristine administration. The expression of IL-6 was increased by vincristine administration and was co-localized in the invading macrophage. Moreover, a neutralizing antibody of IL-6, which was injected into areas surrounding the sciatic nerve on day 0, 3, and 6, significantly attenuated vincristine-induced mechanical allodynia from day 7 to day 28. In addition, the incidence of vincristine-induced mechanical allodynia in IL-6 knockout mice was lower than that in wild type mice from day 3 to day 28. These results suggest that the invading peripheral macrophage-derived IL-6 plays a critical role in vincristine-induced mechanical allodynia. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/18652822/The_critical_role_of_invading_peripheral_macrophage_derived_interleukin_6_in_vincristine_induced_mechanical_allodynia_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(08)00731-0 DB - PRIME DP - Unbound Medicine ER -