Involvement of CC Chemokine Receptor 1 and CCL3 in Acute and Chronic Inflammatory Pain in Mice

Autor:	Sara González-Rodríguez, Luis Menéndez, Ana Baamonde, Ana Lastra, Agustín Hidalgo, María Teresa Fernández-García, María Llorián-Salvador
Rok vydání:	2016
Předmět:	Male 0301 basic medicine CCR1 Chemokine Neutrophils Freund's Adjuvant Anti-Inflammatory Agents Receptors CCR1 Pharmacology Carrageenan Toxicology CCL5 Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals RNA Messenger Chemokine CCL5 Chemokine CCL3 Inflammation Analgesics Dose-Response Relationship Drug biology business.industry General Medicine respiratory system Acute Pain Disease Models Animal 030104 developmental biology Allodynia Spinal Cord Xanthenes chemistry Hyperalgesia Freund's adjuvant biology.protein Chronic Pain medicine.symptom business CC chemokine receptors 030217 neurology & neurosurgery
Zdroj:	Basic & Clinical Pharmacology & Toxicology. 119:32-40
ISSN:	1742-7835
Popis:	Chemokines are chemotactic cytokines whose involvement in nociceptive processing is being increasingly recognized. Based on the previous description of the involvement of CC chemokine receptor type 1 (CCR1) in pathological pain, we have assessed the participation of CCR1 and its endogenous ligands CCL3 and CCL5 in hyperalgesia and allodynia in mice after acute inflammation with carrageenan and chronic inflammation with complete Freund's adjuvant (CFA). The subcutaneous administration of the CCR1 antagonist J113863 (3-30 mg/kg; 30 min. before) dose dependently inhibited carrageenan- and CFA-evoked thermal hyperalgesia and mechanical allodynia produced by CFA, but not by carrageenan. The maximal dose of J113863 did not modify the increase in paw thickness induced by carrageenan or CFA. An almost ten times augmentation of CCL3 levels was detected by ELISA assays in both carrageenan and CFA paws, but not in spinal cords of inflamed mice, whereas CCL5 concentrations remained unaltered. Accordingly, a marked increase of CCL3 mRNA expression was observed in inflamed paws, with CCL3 protein detected in neutrophils and macrophages by immunohistochemical experiments. The intraplantar administration of an anti-CCL3 antibody (0.3-3 μg) blocked thermal hyperalgesia in carrageenan- and CFA-inflamed mice as well as CFA-evoked mechanical allodynia. Our data suggest that the increased concentrations of CCL3 present in inflamed tissues can be involved in acute and chronic inflammatory hyperalgesia as well as in chronic mechanical allodynia, and that these hypernociceptive symptoms can be counteracted by its neutralization with an antibody or by the blockade of CCR1 receptors.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::80842dc75e7a4afa12372d23f87f0478 https://doi.org/10.1111/bcpt.12543 Zobrazit plný text záznamu Plný text ve formátu PDF Plný text ve formátu HTML
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