Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/243214
Type: Artigo
Title: Peripheral neurokinin-1 receptors contribute to kaolin-induced acute monoarthritis in rats
Author: Camargo, Livia L.
Denadai-Souza, Alexandre
Yshii, Lidia M.
Mesquita, Filiphe P.N.
Soares, Antonio G.
Lima, Carla
Schenka, André
Grant, Andrew
Fernandes, Elizabeth
Muscará, Marcelo N.
Costa, Soraia K.P.
Abstract: Objective: intra-articular co-injection of kaolin with carrageenan (CGN) in rodents is widely used as an experimental model of arthritis. However, the ability of kaolin to cause arthritis and related immune responses when administered alone is unclear. We evaluated the contribution of prostanoids and sensory C-fibres (and their neuropeptide substance P) to kaolin-induced inflammation in the rat knee. Methods: Wistar rats, 8-10 weeks old, received an intra-articular injection of kaolin (1-10 mu g/joint) or saline into the knee joint. Knee inflammation, proinflammatory cytokines, pain behaviour and secondary tactile allodynia were assessed over 5 h, when synovial leukocyte counts, histopathological changes and proinflammatory cytokine levels were evaluated. Results: The intra-articular injection of kaolin caused a dose- and time-dependent knee swelling and impairment of motion that were associated with secondary tactile allodynia, elevated concentrations of IL-1 beta, IL-6 and TNF alpha, leukocyte infiltration, and histopathological changes in the ipsilateral hindpaw. The neurokinin-1 (NK1) receptor antagonist SR140333 or neonatal treatment with capsaicin markedly reduced the inflammatory parameters, cytokines and allodynia but failed to significantly inhibit the impaired motion. The cyclo-oxygenase inhibitor indomethacin partially inhibited knee oedema and allodynia but did not affect the leukocyte influx, myeloperoxidase activity or impaired motion in the kaolin-injected rat. Conclusions: We show the first evidence that intra-articular injection of kaolin without CGN produced severe acute monoarthritis. This was highly dependent on substance P (released from C-fibres) and NK1 receptor activation, which stimulated local production of proinflammatory cytokines. This model may be of critical importance for mechanistic studies and screening new anti-inflammatory/analgesic drugs. (C) 2015 S. Karger AG, Basel
Intra-articular co-injection of kaolin with carrageenan (CGN) in rodents is widely used as an experimental model of arthritis. However, the ability of kaolin to cause arthritis and related immune responses when administered alone is unclear. We evaluated the contribution of prostanoids and sensory C-fibres (and their neuropeptide substance P) to kaolin-induced inflammation in the rat knee. Methods: Wistar rats, 8-10 weeks old, received an intra-articular injection of kaolin (1-10 mu g/joint) or saline into the knee joint. Knee inflammation, proinflammatory cytokines, pain behaviour and secondary tactile allodynia were assessed over 5 h, when synovial leukocyte counts, histopathological changes and proinflammatory cytokine levels were evaluated. Results: The intra-articular injection of kaolin caused a dose- and time-dependent knee swelling and impairment of motion that were associated with secondary tactile allodynia, elevated concentrations of IL-1 beta, IL-6 and TNF alpha, leukocyte infiltration, and histopathological changes in the ipsilateral hindpaw. The neurokinin-1 (NK1) receptor antagonist SR140333 or neonatal treatment with capsaicin markedly reduced the inflammatory parameters, cytokines and allodynia but failed to significantly inhibit the impaired motion. The cyclo-oxygenase inhibitor indomethacin partially inhibited knee oedema and allodynia but did not affect the leukocyte influx, myeloperoxidase activity or impaired motion in the kaolin-injected rat. Conclusions: We show the first evidence that intra-articular injection of kaolin without CGN produced severe acute monoarthritis. This was highly dependent on substance P (released from C-fibres) and NK1 receptor activation, which stimulated local production of proinflammatory cytokines. This model may be of critical importance for mechanistic studies and screening new anti-inflammatory/analgesic drugs
Subject: Capsaicina
Prostaglandina-endoperóxido sintases
Dor
Indometacina
Country: Suiça
Editor: Karger
Citation: Peripheral Neurokinin-1 Receptors Contribute To Kaolin-induced Acute Monoarthritis In Rats. Karger, v. 22, p. 373-384 2015.
Rights: Fechado
Identifier DOI: 10.1159/000381549
Address: http://www.karger.com/Article/FullText/381549
Date Issue: 2015
Appears in Collections:FCM - Artigos e Outros Documentos

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