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Article ; Online: An inventory of adjuvants used for vaccination in horses: the past, the present and the future.

Carnet, Flora / Perrin-Cocon, Laure / Paillot, Romain / Lotteau, Vincent / Pronost, Stéphane / Vidalain, Pierre-Olivier

2023 Volume 54, Issue 1, Page(s) 18

Abstract: Vaccination is one of the most widely used strategies to protect horses against pathogens. However, available equine vaccines often have limitations, as they do not always provide effective, long-term protection and booster injections are often required. ...

Abstract	Vaccination is one of the most widely used strategies to protect horses against pathogens. However, available equine vaccines often have limitations, as they do not always provide effective, long-term protection and booster injections are often required. In addition, research efforts are needed to develop effective vaccines against emerging equine pathogens. In this review, we provide an inventory of approved adjuvants for equine vaccines worldwide, and discuss their composition and mode of action when available. A wide range of adjuvants are used in marketed vaccines for horses, the main families being aluminium salts, emulsions, polymers, saponins and ISCOMs. We also present veterinary adjuvants that are already used for vaccination in other species and are currently evaluated in horses to improve equine vaccination and to meet the expected level of protection against pathogens in the equine industry. Finally, we discuss new adjuvants such as liposomes, polylactic acid polymers, inulin, poly-ε-caprolactone nanoparticles and co-polymers that are in development. Our objective is to help professionals in the horse industry understand the composition of marketed equine vaccines in a context of mistrust towards vaccines. Besides, this review provides researchers with a list of adjuvants, either approved or at least evaluated in horses, that could be used either alone or in combination to develop new vaccines.
MeSH term(s)	Horses ; Animals ; Adjuvants, Immunologic/pharmacology ; Vaccination/veterinary ; Nanoparticles/therapeutic use ; Polymers
Chemical Substances	Adjuvants, Immunologic ; Polymers
Language	English
Publishing date	2023-03-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1146298-x
ISSN	1297-9716 ; 0928-4249
ISSN (online)	1297-9716
ISSN	0928-4249
DOI	10.1186/s13567-023-01151-3
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Article ; Online: What role for cellular metabolism in the control of hepatitis viruses?

Diaz, Olivier / Vidalain, Pierre-Olivier / Ramière, Christophe / Lotteau, Vincent / Perrin-Cocon, Laure

Frontiers in immunology

2022 Volume 13, Page(s) 1033314

Abstract: Hepatitis B, C and D viruses (HBV, HCV, HDV, respectively) specifically infect human hepatocytes and often establish chronic viral infections of the liver, thus escaping antiviral immunity for years. Like other viruses, hepatitis viruses rely on the ... ...

Abstract	Hepatitis B, C and D viruses (HBV, HCV, HDV, respectively) specifically infect human hepatocytes and often establish chronic viral infections of the liver, thus escaping antiviral immunity for years. Like other viruses, hepatitis viruses rely on the cellular machinery to meet their energy and metabolite requirements for replication. Although this was initially considered passive parasitism, studies have shown that hepatitis viruses actively rewire cellular metabolism through molecular interactions with specific enzymes such as glucokinase, the first rate-limiting enzyme of glycolysis. As part of research efforts in the field of immunometabolism, it has also been shown that metabolic changes induced by viruses could have a direct impact on the innate antiviral response. Conversely, detection of viral components by innate immunity receptors not only triggers the activation of the antiviral defense but also induces in-depth metabolic reprogramming that is essential to support immunological functions. Altogether, these complex triangular interactions between viral components, innate immunity and hepatocyte metabolism may explain why chronic hepatitis infections progressively lead to liver inflammation and progression to cirrhosis, fibrosis and hepatocellular carcinoma (HCC). In this manuscript, we first present a global overview of known connections between the innate antiviral response and cellular metabolism. We then report known molecular mechanisms by which hepatitis viruses interfere with cellular metabolism in hepatocytes and discuss potential consequences on the innate immune response. Finally, we present evidence that drugs targeting hepatocyte metabolism could be used as an innovative strategy not only to deprive viruses of key metabolites, but also to restore the innate antiviral response that is necessary to clear infection.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular ; Liver Neoplasms ; Hepatitis Viruses ; Hepatocytes ; Antiviral Agents/therapeutic use
Chemical Substances	Antiviral Agents
Language	English
Publishing date	2022-11-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.1033314
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Article ; Online: Rôle du métabolisme cellulaire dans le contrôle des hépatites virales chroniques.

Diaz, Olivier / Legrand, Anne-Flore / El-Orch, Walid / Jacolin, Florentine / Lotteau, Vincent / Ramière, Christophe / Vidalain, Pierre-Olivier / Perrin-Cocon, Laure

Medecine sciences : M/S

2023 Volume 39, Issue 10, Page(s) 754–762

Abstract: Hepatitis viruses modify the cellular metabolism of hepatocytes by interacting with specific enzymes such as glucokinase. The metabolic changes induced by viruses can have a direct impact on the innate antiviral response. The complex interactions between ...

Title translation	Role of cellular metabolism in the control of chronic viral hepatitis.
Abstract	Hepatitis viruses modify the cellular metabolism of hepatocytes by interacting with specific enzymes such as glucokinase. The metabolic changes induced by viruses can have a direct impact on the innate antiviral response. The complex interactions between viral components, innate immunity, and hepatocyte metabolism explain why chronic hepatitis infections lead to liver inflammation, progressing to cirrhosis, fibrosis, and hepatocellular carcinoma. Metabolic regulators could be used in innovative therapies to deprive viruses of key metabolites and induce an antiviral defense.
MeSH term(s)	Humans ; Hepatitis, Chronic ; Carcinoma, Hepatocellular ; Liver Neoplasms ; Hepatitis, Viral, Human ; Antiviral Agents/therapeutic use
Chemical Substances	Antiviral Agents
Language	French
Publishing date	2023-11-09
Publishing country	France
Document type	English Abstract ; Journal Article
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2023125
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Article: Hamster organotypic kidney culture model of early-stage SARS-CoV-2 infection highlights a two-step renal susceptibility.

Shyfrin, Sophie R / Ferren, Marion / Perrin-Cocon, Laure / Espi, Maxime / Charmetant, Xavier / Brailly, Manon / Decimo, Didier / Iampietro, Mathieu / Canus, Lola / Horvat, Branka / Lotteau, Vincent / Vidalain, Pierre-Olivier / Thaunat, Olivier / Mathieu, Cyrille

Journal of tissue engineering

2022 Volume 13, Page(s) 20417314221122130

Abstract: Kidney pathology is frequently reported in patients hospitalized with COVID-19, the pandemic disease caused by the Severe acute respiratory coronavirus 2 (SARS-CoV-2). However, due to a lack of suitable study models, the events occurring in the kidney ... ...

Abstract	Kidney pathology is frequently reported in patients hospitalized with COVID-19, the pandemic disease caused by the Severe acute respiratory coronavirus 2 (SARS-CoV-2). However, due to a lack of suitable study models, the events occurring in the kidney during the earliest stages of infection remain unknown. We have developed hamster organotypic kidney cultures (OKCs) to study the early stages of direct renal infection. OKCs maintained key renal structures in their native three-dimensional arrangement. SARS-CoV-2 productively replicated in hamster OKCs, initially targeting endothelial cells and later disseminating into proximal tubules. We observed a delayed interferon response, markers of necroptosis and pyroptosis, and an early repression of pro-inflammatory cytokines transcription followed by a strong later upregulation. While it remains an open question whether an active replication of SARS-CoV-2 takes place in the kidneys of COVID-19 patients with AKI, our model provides new insights into the kinetics of SARS-CoV-2 kidney infection and can serve as a powerful tool for studying kidney infection by other pathogens and testing the renal toxicity of drugs.
Language	English
Publishing date	2022-09-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2573915-3
ISSN	2041-7314
ISSN	2041-7314
DOI	10.1177/20417314221122130
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Article ; Online: Domain 2 of Hepatitis C Virus Protein NS5A Activates Glucokinase and Induces Lipogenesis in Hepatocytes.

Perrin-Cocon, Laure / Kundlacz, Cindy / Jacquemin, Clémence / Hanoulle, Xavier / Aublin-Gex, Anne / Figl, Marianne / Manteca, Jeremy / André, Patrice / Vidalain, Pierre-Olivier / Lotteau, Vincent / Diaz, Olivier

International journal of molecular sciences

2022 Volume 23, Issue 2

Abstract: Hepatitis C virus (HCV) relies on cellular lipid metabolism for its replication, and actively modulates lipogenesis and lipid trafficking in infected hepatocytes. This translates into an intracellular accumulation of triglycerides leading to liver ... ...

Abstract	Hepatitis C virus (HCV) relies on cellular lipid metabolism for its replication, and actively modulates lipogenesis and lipid trafficking in infected hepatocytes. This translates into an intracellular accumulation of triglycerides leading to liver steatosis, cirrhosis and hepatocellular carcinoma, which are hallmarks of HCV pathogenesis. While the interaction of HCV with hepatocyte metabolic pathways is patent, how viral proteins are able to redirect central carbon metabolism towards lipogenesis is unclear. Here, we report that the HCV protein NS5A activates the glucokinase (GCK) isoenzyme of hexokinases through its D2 domain (NS5A-D2). GCK is the first rate-limiting enzyme of glycolysis in normal hepatocytes whose expression is replaced by the hexokinase 2 (HK2) isoenzyme in hepatocellular carcinoma cell lines. We took advantage of a unique cellular model specifically engineered to re-express GCK instead of HK2 in the Huh7 cell line to evaluate the consequences of NS5A-D2 expression on central carbon and lipid metabolism. NS5A-D2 increased glucose consumption but decreased glycogen storage. This was accompanied by an altered mitochondrial respiration, an accumulation of intracellular triglycerides and an increased production of very-low density lipoproteins. Altogether, our results show that NS5A-D2 can reprogram central carbon metabolism towards a more energetic and glycolytic phenotype compatible with HCV needs for replication.
MeSH term(s)	Cell Line, Tumor ; Gene Knockdown Techniques ; Glucokinase/metabolism ; Glycogen/metabolism ; Glycolysis ; Hepacivirus/physiology ; Hepatitis C/metabolism ; Hepatitis C/virology ; Hepatocytes/metabolism ; Hepatocytes/virology ; Host-Pathogen Interactions ; Humans ; Lipid Metabolism ; Lipogenesis ; Mitochondria/metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; RNA-Dependent RNA Polymerase/chemistry ; RNA-Dependent RNA Polymerase/metabolism ; Viral Nonstructural Proteins/chemistry ; Viral Nonstructural Proteins/metabolism
Chemical Substances	Viral Nonstructural Proteins ; Glycogen (9005-79-2) ; Glucokinase (EC 2.7.1.2) ; NS-5 protein, hepatitis C virus (EC 2.7.7.48) ; RNA-Dependent RNA Polymerase (EC 2.7.7.48)
Language	English
Publishing date	2022-01-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23020919
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Article ; Online: The current landscape of coronavirus-host protein-protein interactions.

Perrin-Cocon, Laure / Diaz, Olivier / Jacquemin, Clémence / Barthel, Valentine / Ogire, Eva / Ramière, Christophe / André, Patrice / Lotteau, Vincent / Vidalain, Pierre-Olivier

Journal of translational medicine

2020 Volume 18, Issue 1, Page(s) 319

Abstract: In less than 20 years, three deadly coronaviruses, SARS-CoV, MERS-CoV and SARS-CoV-2, have emerged in human population causing hundreds to hundreds of thousands of deaths. Other coronaviruses are causing epizootic representing a significant threat for ... ...

Abstract	In less than 20 years, three deadly coronaviruses, SARS-CoV, MERS-CoV and SARS-CoV-2, have emerged in human population causing hundreds to hundreds of thousands of deaths. Other coronaviruses are causing epizootic representing a significant threat for both domestic and wild animals. Members of this viral family have the longest genome of all RNA viruses, and express up to 29 proteins establishing complex interactions with the host proteome. Deciphering these interactions is essential to identify cellular pathways hijacked by these viruses to replicate and escape innate immunity. Virus-host interactions also provide key information to select targets for antiviral drug development. Here, we have manually curated the literature to assemble a unique dataset of 1311 coronavirus-host protein-protein interactions. Functional enrichment and network-based analyses showed coronavirus connections to RNA processing and translation, DNA damage and pathogen sensing, interferon production, and metabolic pathways. In particular, this global analysis pinpointed overlooked interactions with translation modulators (GIGYF2-EIF4E2), components of the nuclear pore, proteins involved in mitochondria homeostasis (PHB, PHB2, STOML2), and methylation pathways (MAT2A/B). Finally, interactome data provided a rational for the antiviral activity of some drugs inhibiting coronaviruses replication. Altogether, this work describing the current landscape of coronavirus-host interactions provides valuable hints for understanding the pathophysiology of coronavirus infections and developing effective antiviral therapies.
MeSH term(s)	Animals ; Betacoronavirus/physiology ; COVID-19 ; Coronavirus/chemistry ; Coronavirus/metabolism ; Coronavirus Infections/metabolism ; Coronavirus Infections/virology ; Databases, Protein ; Host-Pathogen Interactions/physiology ; Humans ; Mitochondrial Proteins/metabolism ; Pandemics ; Pneumonia, Viral/metabolism ; Pneumonia, Viral/virology ; Protein Interaction Maps ; SARS-CoV-2 ; Transcription Factors/metabolism ; Viral Proteins/metabolism ; Virus Replication/genetics
Chemical Substances	Mitochondrial Proteins ; Transcription Factors ; Viral Proteins
Keywords	covid19
Language	English
Publishing date	2020-08-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1479-5876
ISSN (online)	1479-5876
DOI	10.1186/s12967-020-02480-z
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Article ; Online: Targeting the liver X receptor with dendrogenin A differentiates tumour cells to secrete immunogenic exosome-enriched vesicles.

Record, Michel / Attia, Mehdi / Carayon, Kevin / Pucheu, Laly / Bunay, Julio / Soulès, Régis / Ayadi, Silia / Payré, Bruno / Perrin-Cocon, Laure / Bourgailh, Florence / Lamazière, Antonin / Lotteau, Vincent / Poirot, Marc / Silvente-Poirot, Sandrine / de Medina, Philippe

Journal of extracellular vesicles

2022 Volume 11, Issue 4, Page(s) e12211

Abstract: Tumour cells are characterized by having lost their differentiation state. They constitutively secrete small extracellular vesicles (sEV) called exosomes when they come from late endosomes. Dendrogenin A (DDA) is an endogenous tumour suppressor ... ...

Abstract	Tumour cells are characterized by having lost their differentiation state. They constitutively secrete small extracellular vesicles (sEV) called exosomes when they come from late endosomes. Dendrogenin A (DDA) is an endogenous tumour suppressor cholesterol-derived metabolite. It is a new class of ligand of the nuclear Liver X receptors (LXR) which regulate cholesterol homeostasis and immunity. We hypothesized that DDA, which induces tumour cell differentiation, inhibition of tumour growth and immune cell infiltration into tumours, could functionally modify sEV secreted by tumour cells. Here, we have shown that DDA differentiates tumour cells by acting on the LXRβ. This results in an increased production of sEV (DDA-sEV) which includes exosomes. The DDA-sEV secreted from DDA-treated cells were characterized for their content and activity in comparison to sEV secreted from control cells (C-sEV). DDA-sEV were enriched, relatively to C-sEV, in several proteins and lipids such as differentiation antigens, "eat-me" signals, lipidated LC3 and the endosomal phospholipid bis(monoacylglycero)phosphate, which stimulates dendritic cell maturation and a Th1 T lymphocyte polarization. Moreover, DDA-sEV inhibited the growth of tumours implanted into immunocompetent mice compared to control conditions. This study reveals a pharmacological control through a nuclear receptor of exosome-enriched tumour sEV secretion, composition and immune function. Targeting the LXR may be a novel way to reprogram tumour cells and sEV to stimulate immunity against cancer.
MeSH term(s)	Animals ; Cholestanols ; Cholesterol/metabolism ; Exosomes/metabolism ; Imidazoles ; Liver X Receptors/metabolism ; Mice ; Neoplasms/drug therapy
Chemical Substances	5-hydroxy-6-(2-(1H-imidazol-4-yl)ethylamino)cholestan-3-ol ; Cholestanols ; Imidazoles ; Liver X Receptors ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2022-06-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2683797-3
ISSN	2001-3078 ; 2001-3078
ISSN (online)	2001-3078
ISSN	2001-3078
DOI	10.1002/jev2.12211
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Article ; Online: Domain 2 of Hepatitis C Virus Protein NS5A Activates Glucokinase and Induces Lipogenesis in Hepatocytes

Laure Perrin-Cocon / Cindy Kundlacz / Clémence Jacquemin / Xavier Hanoulle / Anne Aublin-Gex / Marianne Figl / Jeremy Manteca / Patrice André / Pierre-Olivier Vidalain / Vincent Lotteau / Olivier Diaz

International Journal of Molecular Sciences, Vol 23, Iss 919, p

2022 Volume 919

Abstract	Hepatitis C virus (HCV) relies on cellular lipid metabolism for its replication, and actively modulates lipogenesis and lipid trafficking in infected hepatocytes. This translates into an intracellular accumulation of triglycerides leading to liver steatosis, cirrhosis and hepatocellular carcinoma, which are hallmarks of HCV pathogenesis. While the interaction of HCV with hepatocyte metabolic pathways is patent, how viral proteins are able to redirect central carbon metabolism towards lipogenesis is unclear. Here, we report that the HCV protein NS5A activates the glucokinase (GCK) isoenzyme of hexokinases through its D2 domain (NS5A-D2). GCK is the first rate-limiting enzyme of glycolysis in normal hepatocytes whose expression is replaced by the hexokinase 2 (HK2) isoenzyme in hepatocellular carcinoma cell lines. We took advantage of a unique cellular model specifically engineered to re-express GCK instead of HK2 in the Huh7 cell line to evaluate the consequences of NS5A-D2 expression on central carbon and lipid metabolism. NS5A-D2 increased glucose consumption but decreased glycogen storage. This was accompanied by an altered mitochondrial respiration, an accumulation of intracellular triglycerides and an increased production of very-low density lipoproteins. Altogether, our results show that NS5A-D2 can reprogram central carbon metabolism towards a more energetic and glycolytic phenotype compatible with HCV needs for replication.
Keywords	hepatitis C virus ; NS5A ; glycolysis ; glucokinase ; lipogenesis ; human lipoprotein ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	570
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: The current landscape of coronavirus-host protein–protein interactions

Laure Perrin-Cocon / Olivier Diaz / Clémence Jacquemin / Valentine Barthel / Eva Ogire / Christophe Ramière / Patrice André / Vincent Lotteau / Pierre-Olivier Vidalain

Journal of Translational Medicine, Vol 18, Iss 1, Pp 1-

2020 Volume 15

Abstract: Abstract In less than 20 years, three deadly coronaviruses, SARS-CoV, MERS-CoV and SARS-CoV-2, have emerged in human population causing hundreds to hundreds of thousands of deaths. Other coronaviruses are causing epizootic representing a significant ... ...

Abstract	Abstract In less than 20 years, three deadly coronaviruses, SARS-CoV, MERS-CoV and SARS-CoV-2, have emerged in human population causing hundreds to hundreds of thousands of deaths. Other coronaviruses are causing epizootic representing a significant threat for both domestic and wild animals. Members of this viral family have the longest genome of all RNA viruses, and express up to 29 proteins establishing complex interactions with the host proteome. Deciphering these interactions is essential to identify cellular pathways hijacked by these viruses to replicate and escape innate immunity. Virus-host interactions also provide key information to select targets for antiviral drug development. Here, we have manually curated the literature to assemble a unique dataset of 1311 coronavirus-host protein–protein interactions. Functional enrichment and network-based analyses showed coronavirus connections to RNA processing and translation, DNA damage and pathogen sensing, interferon production, and metabolic pathways. In particular, this global analysis pinpointed overlooked interactions with translation modulators (GIGYF2-EIF4E2), components of the nuclear pore, proteins involved in mitochondria homeostasis (PHB, PHB2, STOML2), and methylation pathways (MAT2A/B). Finally, interactome data provided a rational for the antiviral activity of some drugs inhibiting coronaviruses replication. Altogether, this work describing the current landscape of coronavirus-host interactions provides valuable hints for understanding the pathophysiology of coronavirus infections and developing effective antiviral therapies.
Keywords	SARS-CoV-2 ; Coronavirus ; Interactome ; Virus-host interactions ; Protein–protein interactions ; Medicine ; R
Language	English
Publishing date	2020-08-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article ; Online: Toll-like Receptor 4-Induced Glycolytic Burst in Human Monocyte-Derived Dendritic Cells Results from p38-Dependent Stabilization of HIF-1α and Increased Hexokinase II Expression.

Perrin-Cocon, Laure / Aublin-Gex, Anne / Diaz, Olivier / Ramière, Christophe / Peri, Francesco / André, Patrice / Lotteau, Vincent

Journal of immunology (Baltimore, Md. : 1950)

2018 Volume 201, Issue 5, Page(s) 1510–1521

Abstract: Cell metabolism now appears as an essential regulator of immune cells activation. In particular, TLR stimulation triggers metabolic reprogramming of dendritic cells (DCs) with an increased glycolytic flux, whereas inhibition of glycolysis alters their ... ...

Abstract	Cell metabolism now appears as an essential regulator of immune cells activation. In particular, TLR stimulation triggers metabolic reprogramming of dendritic cells (DCs) with an increased glycolytic flux, whereas inhibition of glycolysis alters their functional activation. The molecular mechanisms involved in the control of glycolysis upon TLR stimulation are poorly understood for human DCs. TLR4 activation of human monocyte-derived DCs (MoDCs) stimulated glycolysis with an increased glucose consumption and lactate production. Global hexokinase (HK) activity, controlling the initial rate-limiting step of glycolysis, was also increased. TLR4-induced glycolytic burst correlated with a differential modulation of HK isoenzymes. LPS strongly enhanced the expression of HK2, whereas HK3 was reduced, HK1 remained unchanged, and HK4 was not expressed. Expression of the other rate-limiting glycolytic enzymes was not significantly increased. Exploring the signaling pathways involved in LPS-induced glycolysis with various specific inhibitors, we observed that only the inhibitors of p38-MAPK (SB203580) and of HIF-1α DNA binding (echinomycin) reduced both the glycolytic activity and production of cytokines triggered by TLR4 stimulation. In addition, LPS-induced HK2 expression required p38-MAPK-dependent HIF-1α accumulation and transcriptional activity. TLR1/2 and TLR2/6 stimulation increased glucose consumption by MoDCs through alternate mechanisms that are independent of p38-MAPK activation. TBK1 contributed to glycolysis regulation when DCs were stimulated via TLR2/6. Therefore, our results indicate that TLR4-dependent upregulation of glycolysis in human MoDCs involves a p38-MAPK-dependent HIF-1α accumulation, leading to an increased HK activity supported by enhanced HK2 expression.
MeSH term(s)	Cells, Cultured ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Gene Expression Regulation, Enzymologic/drug effects ; Gene Expression Regulation, Enzymologic/immunology ; Hexokinase/immunology ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/immunology ; Lipopolysaccharides/toxicity ; Monocytes/immunology ; Monocytes/pathology ; Protein Stability ; Toll-Like Receptor 4/agonists ; Toll-Like Receptor 4/immunology ; p38 Mitogen-Activated Protein Kinases/immunology
Chemical Substances	HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Lipopolysaccharides ; TLR4 protein, human ; Toll-Like Receptor 4 ; lipopolysaccharide, Escherichia coli O111 B4 ; HK2 protein, human (EC 2.7.1.1) ; Hexokinase (EC 2.7.1.1) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2018-07-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1701522
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