Role of T CD4+ cells, macrophages, C-low ...
Type de document :
Compte-rendu et recension critique d'ouvrage
DOI :
PMID :
Titre :
Role of T CD4+ cells, macrophages, C-low threshold mechanoreceptors and spinal Cav3.2 channels in inflammation and related pain-like symptoms in murine inflammatory models
Auteur(s) :
Picard, Elodie [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Kerckhove, Nicolas [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
CHU Clermont-Ferrand
François, Amaury [Auteur]
Institut de Génomique Fonctionnelle [IGF]
Boudieu, Ludivine [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Billard, Elisabeth [Auteur]
Université Clermont Auvergne [UCA]
Carvalho, Frédéric Antonio [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Bogard, Gemma [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Gosset, Philippe [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Bourdier, Justine [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Aissouni, Youssef [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Bourinet, Emmanuel [Auteur]
Institut de Génomique Fonctionnelle [IGF]
Eschalier, Alain [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Daulhac, Laurence [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Mallet, Christophe [Auteur correspondant]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Kerckhove, Nicolas [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
CHU Clermont-Ferrand
François, Amaury [Auteur]
Institut de Génomique Fonctionnelle [IGF]
Boudieu, Ludivine [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Billard, Elisabeth [Auteur]
Université Clermont Auvergne [UCA]
Carvalho, Frédéric Antonio [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Bogard, Gemma [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Gosset, Philippe [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Bourdier, Justine [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Aissouni, Youssef [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Bourinet, Emmanuel [Auteur]
Institut de Génomique Fonctionnelle [IGF]
Eschalier, Alain [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Daulhac, Laurence [Auteur]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Mallet, Christophe [Auteur correspondant]
Neuro-Dol [Neuro-Dol]
Institut Analgesia
Titre de la revue :
British Journal of Pharmacology
Pagination :
385-400
Éditeur :
Wiley
Date de publication :
2023
ISSN :
0007-1188
Mot(s)-clé(s) en anglais :
T-type calcium channels
inflammation
inflammatory pain
mechanical hypersensitivity
pharmacology
inflammation
inflammatory pain
mechanical hypersensitivity
pharmacology
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Sciences du Vivant [q-bio]/Immunologie
Sciences du Vivant [q-bio]/Neurosciences [q-bio.NC]
Sciences du Vivant [q-bio]/Immunologie
Sciences du Vivant [q-bio]/Neurosciences [q-bio.NC]
Résumé en anglais : [en]
Background and purpose: T-type calcium channels, mainly the Cav 3.2 subtype, are important contributors to the nociceptive signaling pathway. We investigated their involvement in inflammation and related pain-like ...
Lire la suite >Background and purpose: T-type calcium channels, mainly the Cav 3.2 subtype, are important contributors to the nociceptive signaling pathway. We investigated their involvement in inflammation and related pain-like symptoms.Experimental approach: The involvement of Cav 3.2 and T-type channels was investigated using genetic and pharmacological inhibition to assess mechanical allodynia/hyperalgesia and edema development in two murine inflammatory pain models. The location of Cav 3.2 involved in pain-like symptoms was studied in mice with Cav 3.2 knocked out in C-low threshold mechanoreceptors (C-LTMR) and the use of ABT-639, a peripherally restricted T-type channel inhibitor. The anti-edematous effect of Cav 3.2 inhibition was investigated in chimeric mice with immune cells deleted for Cav 3.2. Lymphocytes and macrophages from either green fluorescent protein-targeted Cav 3.2 or KO mice were used to determine the expression of Cav 3.2 protein and the functional status of the cells.Key results: We showed the role of Cav 3.2 channels in the development of pain-like symptoms and edema in the two murine inflammatory pain models. For the first time, we provide evidence of the involvement of Cav 3.2 channels located on C-LTMRs and spinal cord in inflammatory pain. We showed that Cav 3.2 channels located in T cells and macrophages contribute to the inflammatory process.Conclusion and implications: This work highlights the crucial role of Cav 3.2 channels in inflammation and related pain and suggests that targeting Cav 3.2 channels with pharmacological agents could be an attractive and readily evaluable strategy in a clinical trial to relieve chronic inflammatory pain in affected patients.Lire moins >
Lire la suite >Background and purpose: T-type calcium channels, mainly the Cav 3.2 subtype, are important contributors to the nociceptive signaling pathway. We investigated their involvement in inflammation and related pain-like symptoms.Experimental approach: The involvement of Cav 3.2 and T-type channels was investigated using genetic and pharmacological inhibition to assess mechanical allodynia/hyperalgesia and edema development in two murine inflammatory pain models. The location of Cav 3.2 involved in pain-like symptoms was studied in mice with Cav 3.2 knocked out in C-low threshold mechanoreceptors (C-LTMR) and the use of ABT-639, a peripherally restricted T-type channel inhibitor. The anti-edematous effect of Cav 3.2 inhibition was investigated in chimeric mice with immune cells deleted for Cav 3.2. Lymphocytes and macrophages from either green fluorescent protein-targeted Cav 3.2 or KO mice were used to determine the expression of Cav 3.2 protein and the functional status of the cells.Key results: We showed the role of Cav 3.2 channels in the development of pain-like symptoms and edema in the two murine inflammatory pain models. For the first time, we provide evidence of the involvement of Cav 3.2 channels located on C-LTMRs and spinal cord in inflammatory pain. We showed that Cav 3.2 channels located in T cells and macrophages contribute to the inflammatory process.Conclusion and implications: This work highlights the crucial role of Cav 3.2 channels in inflammation and related pain and suggests that targeting Cav 3.2 channels with pharmacological agents could be an attractive and readily evaluable strategy in a clinical trial to relieve chronic inflammatory pain in affected patients.Lire moins >
Langue :
Anglais
Vulgarisation :
Non
Projet ANR :
Source :