Blockade of Store-Operated Calcium Entry Reduces IL-17/TNF Cytokine-Induced Inflammatory Response in Human Myoblasts
Autor: | Audrey Beringer, Yves Gouriou, Fabien Lavocat, Michel Ovize, Pierre Miossec |
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Přispěvatelé: | Université de Lyon (COMUE), Cardiovasculaire, métabolisme, diabétologie et nutrition (CarMeN), Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Institut National des Sciences Appliquées (INSA)-Université de Lyon-Institut National des Sciences Appliquées (INSA)-Université de Lyon-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Institut National de la Recherche Agronomique (INRA), Hôpital Louis Pradel [CHU - HCL], Hospices Civils de Lyon (HCL), OpeRa IHU program, IHU OPeRa of Universite de Lyon, within the program Investissements d'Avenir ANR-10-IBHU-004, RHU MARVELOUS of Universite de Lyon, within the program Investissements d'Avenir ANR-16-RHUS-0009, Ministry of Education and Research, ProdInra, Migration |
Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: |
interleukine
0301 basic medicine medicine.medical_treatment Cell Communication interleukin-17 0302 clinical medicine Immunologie Immunology and Allergy Myocyte inflammatory myopathies Endoplasmic Reticulum Chaperone BiP Cells Cultured tumor necrosis factor-alpha Original Research Voltage-dependent calcium channel Chemistry myoblasts Store-operated calcium entry 3. Good health Molecular Imaging Cytokine myoblaste [SDV.IMM]Life Sciences [q-bio]/Immunology Tumor necrosis factor alpha medicine.symptom store-operated calcium entry lcsh:Immunologic diseases. Allergy medicine.medical_specialty [SDV.IMM] Life Sciences [q-bio]/Immunology Immunology Inflammation Peripheral blood mononuclear cell nécrose tumorale 03 medical and health sciences Internal medicine medicine Humans myopathie Chemokine CCL20 Interleukin-6 Mitochondria Muscle Mononuclear cell infiltration Oxidative Stress 030104 developmental biology Endocrinology Leukocytes Mononuclear Calcium Calcium Channels tumor necrosis factor-α lcsh:RC581-607 030215 immunology |
Zdroj: | Frontiers in Immunology, Vol 9 (2019) Frontiers in Immunology Frontiers in Immunology, Frontiers, 2019, 9, ⟨10.3389/fimmu.2018.03170⟩ Frontiers in Immunology (9), . (2019) |
ISSN: | 1664-3224 |
DOI: | 10.3389/fimmu.2018.03170/full |
Popis: | International audience; Muscle inflammation as in idiopathic inflammatory myopathies (IIM) leads to muscle weakness, mononuclear cell infiltration, and myofiber dysfunction affecting calcium channels. The effects of interleukin-17A (IL-17) and tumor necrosis factor-alpha (TNF alpha) on inflammation and calcium changes were investigated in human myoblasts. Human myoblasts were exposed to IL-17 and/or TNF alpha with/without store-operated Ca2+ entry (SOCE) inhibitors (2-ABP or BTP2). For co-cultures, peripheral blood mononuclear cells (PBMC) from healthy donors activated or not with phytohemagglutinin (PHA) were added to myoblasts at a 5:1 ratio. IL-17 and TNF alpha induced in synergy CCL20 and IL-6 production by myoblasts (> 14-fold). PBMC-myoblast co-cultures enhanced CCL20 and IL-6 production in the presence or not of PHA compared to PBMC or myoblast monocultures. Anti-IL-17 and/or anti-TNF alpha decreased the production of IL-6 in co-cultures (p < 0.05). Transwell system that prevents direct cell-cell contact reduced CCL20 (p < 0.01) but not IL-6 secretion. IL-17 and/or TNF alpha increased the level of the ER stress marker Grp78, mitochondrial ROS and promoted SOCE activation by 2-fold (p < 0.01) in isolated myoblasts. SOCE inhibitors reduced the IL-6 production induced by IL-17/TNF alpha. Therefore, muscle inflammation induced by IL-17 and/or TNF alpha may increase muscle cell dysfunction, which, in turn, increased inflammation. Such close interplay between immune and non-immune mechanisms may drive and increase muscle inflammation and weakness. |
Databáze: | OpenAIRE |
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