دورية أكاديمية
Glycolytic reprogramming of macrophages activated by NOD1 and TLR4 agonists: No association with proinflammatory cytokine production in normoxia.
| العنوان: | Glycolytic reprogramming of macrophages activated by NOD1 and TLR4 agonists: No association with proinflammatory cytokine production in normoxia. |
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| المؤلفون: | Murugina NE; Laboratory of Clinical Immunology, National Research Center, Institute of Immunology, Federal Medical-Biological Agency of Russia, Kashirskoe shosse 24, 115522 Moscow, Russia., Budikhina AS; Laboratory of Clinical Immunology, National Research Center, Institute of Immunology, Federal Medical-Biological Agency of Russia, Kashirskoe shosse 24, 115522 Moscow, Russia., Dagil YA; Laboratory of Clinical Immunology, National Research Center, Institute of Immunology, Federal Medical-Biological Agency of Russia, Kashirskoe shosse 24, 115522 Moscow, Russia., Maximchik PV; Faculty of Fundamental Medicine, Lomonosov Moscow State University, Leninskie Gory 1, 119991 Moscow, Russia., Balyasova LS; Laboratory of Clinical Immunology, National Research Center, Institute of Immunology, Federal Medical-Biological Agency of Russia, Kashirskoe shosse 24, 115522 Moscow, Russia., Murugin VV; Laboratory of Clinical Immunology, National Research Center, Institute of Immunology, Federal Medical-Biological Agency of Russia, Kashirskoe shosse 24, 115522 Moscow, Russia., Melnikov MV; Laboratory of Clinical Immunology, National Research Center, Institute of Immunology, Federal Medical-Biological Agency of Russia, Kashirskoe shosse 24, 115522 Moscow, Russia; Department of Neurology, Neurosurgery and Medical Genetics, Pirogov Russian National Research Medical University, Ostrovityanova street 1, 117997 Moscow, Russia., Sharova VS; Koltsov Institute of Developmental Biology, Russian Academy of Sciences, Vavilova street 26, 119334 Moscow, Russia., Nikolaeva AM; Laboratory of Clinical Immunology, National Research Center, Institute of Immunology, Federal Medical-Biological Agency of Russia, Kashirskoe shosse 24, 115522 Moscow, Russia; Biological Faculty, Lomonosov Moscow State University, Leninskie Gory 1, 119991 Moscow, Russia., Chkadua GZ; Laboratory of Experimental Diagnostics and Biotherapy of Tumors, N. N. Blokhin National Medical Research Center of Oncology of the Ministry of Health of the Russian Federation, Kashirskoe shosse 24 Building 2, 115522 Moscow, Russia., Pinegin BV; Laboratory of Clinical Immunology, National Research Center, Institute of Immunology, Federal Medical-Biological Agency of Russia, Kashirskoe shosse 24, 115522 Moscow, Russia., Pashenkov MV; Laboratory of Clinical Immunology, National Research Center, Institute of Immunology, Federal Medical-Biological Agency of Russia, Kashirskoe shosse 24, 115522 Moscow, Russia. Electronic address: mvpashenkov@yandex.ru. |
| المصدر: | The Journal of biological chemistry [J Biol Chem] 2020 Mar 06; Vol. 295 (10), pp. 3099-3114. Date of Electronic Publication: 2020 Jan 31. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology Country of Publication: United States NLM ID: 2985121R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1083-351X (Electronic) Linking ISSN: 00219258 NLM ISO Abbreviation: J Biol Chem Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2021- : [New York, NY] : Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology Original Publication: Baltimore, MD : American Society for Biochemistry and Molecular Biology |
| مواضيع طبية MeSH: | Cytokines/*metabolism , Glycolysis/*drug effects , Lipopolysaccharides/*pharmacology , Macrophages/*metabolism , Nod1 Signaling Adaptor Protein/*agonists , Toll-Like Receptor 4/*agonists, Animals ; Carboxy-Lyases/metabolism ; Cell Hypoxia ; Dendritic Cells/drug effects ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Deoxyglucose/pharmacology ; Humans ; Macrophages/drug effects ; Macrophages/immunology ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice ; Mice, Inbred C57BL ; Monocytes/cytology ; Monocytes/metabolism ; Nod1 Signaling Adaptor Protein/metabolism ; Nod2 Signaling Adaptor Protein/agonists ; Nod2 Signaling Adaptor Protein/metabolism ; Oligomycins/pharmacology ; Proto-Oncogene Proteins c-akt/metabolism ; Toll-Like Receptor 4/metabolism ; Unfolded Protein Response/drug effects |
| مستخلص: | Upon activation with pathogen-associated molecular patterns, metabolism of macrophages and dendritic cells is shifted from oxidative phosphorylation to aerobic glycolysis, which is considered important for proinflammatory cytokine production. Fragments of bacterial peptidoglycan (muramyl peptides) activate innate immune cells through nucleotide-binding oligomerization domain (NOD) 1 and/or NOD2 receptors. Here, we show that NOD1 and NOD2 agonists induce early glycolytic reprogramming of human monocyte-derived macrophages (MDM), which is similar to that induced by the Toll-like receptor 4 (TLR4) agonist lipopolysaccharide. This glycolytic reprogramming depends on Akt kinases, independent of mTOR complex 1 and is efficiently inhibited by 2-deoxy-d-glucose (2-DG) or by glucose starvation. 2-DG inhibits proinflammatory cytokine production by MDM and monocyte-derived dendritic cells activated by NOD1 or TLR4 agonists, except for tumor necrosis factor production by MDM, which is inhibited initially, but augmented 4 h after addition of agonists and later. However, 2-DG exerts these effects by inducing unfolded protein response rather than by inhibiting glycolysis. By contrast, glucose starvation does not cause unfolded protein response and, in normoxic conditions, only marginally affects proinflammatory cytokine production triggered through NOD1 or TLR4. In hypoxia mimicked by treating MDM with oligomycin (a mitochondrial ATP synthase inhibitor), both 2-DG and glucose starvation strongly suppress tumor necrosis factor and interleukin-6 production and compromise cell viability. In summary, the requirement of glycolytic reprogramming for proinflammatory cytokine production in normoxia is not obvious, and effects of 2-DG on cytokine responses should be interpreted cautiously. In hypoxia, however, glycolysis becomes critical for cytokine production and cell survival. (© 2020 Murugina et al.) |
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| فهرسة مساهمة: | Keywords: 2-deoxy-d-glucose; NOD1; NOD2; Nod-like receptor (NLR); cytokine; dendritic cell; glucose metabolism; glycolysis; macrophage; metabolic reprogramming; muramyl peptides; unfolded protein response (UPR) |
| المشرفين على المادة: | 0 (Cytokines) 0 (Lipopolysaccharides) 0 (Nod1 Signaling Adaptor Protein) 0 (Nod2 Signaling Adaptor Protein) 0 (Oligomycins) 0 (Toll-Like Receptor 4) 9G2MP84A8W (Deoxyglucose) EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1) EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) EC 4.1.1.- (ACOD1 protein, human) EC 4.1.1.- (Carboxy-Lyases) |
| تواريخ الأحداث: | Date Created: 20200202 Date Completed: 20201020 Latest Revision: 20210317 |
| رمز التحديث: | 20240628 |
| مُعرف محوري في PubMed: | PMC7062164 |
| DOI: | 10.1074/jbc.RA119.010589 |
| PMID: | 32005665 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1083-351X |
|---|---|
| DOI: | 10.1074/jbc.RA119.010589 |