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Article ; Online: Role of glutathione metabolism in host defense against

Kerstholt, Mariska / Vrijmoeth, Hedwig / Lachmandas, Ekta / Oosting, Marije / Lupse, Mihaela / Flonta, Mirela / Dinarello, Charles A / Netea, Mihai G / Joosten, Leo A B

Proceedings of the National Academy of Sciences of the United States of America

2018 Volume 115, Issue 10, Page(s) E2320–E2328

Abstract: Pathogen-induced changes in host cell metabolism are known to be important for the immune response. In this study, we investigated how infection with the Lyme disease-causing ... ...

Abstract	Pathogen-induced changes in host cell metabolism are known to be important for the immune response. In this study, we investigated how infection with the Lyme disease-causing bacterium
MeSH term(s)	Borrelia burgdorferi/physiology ; Cytokines/genetics ; Cytokines/metabolism ; Glutathione/metabolism ; Host-Pathogen Interactions ; Humans ; Lyme Disease/genetics ; Lyme Disease/metabolism ; Lyme Disease/microbiology ; Monocytes/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	Cytokines ; Reactive Oxygen Species ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2018-02-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1720833115
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Article ; Online: Role of Glutamine Metabolism in Host Defense Against Mycobacterium tuberculosis Infection.

Koeken, Valerie A C M / Lachmandas, Ekta / Riza, Anca / Matzaraki, Vasiliki / Li, Yang / Kumar, Vinod / Oosting, Marije / Joosten, Leo A B / Netea, Mihai G / van Crevel, Reinout

The Journal of infectious diseases

2018 Volume 219, Issue 10, Page(s) 1662–1670

Abstract: Background: Rewiring cellular metabolism is important for activation of immune cells during host defense against Mycobacterium tuberculosis. Glutamine has been implicated as an immunomodulatory nutrient, but its role in the response to M. tuberculosis ... ...

Abstract	Background: Rewiring cellular metabolism is important for activation of immune cells during host defense against Mycobacterium tuberculosis. Glutamine has been implicated as an immunomodulatory nutrient, but its role in the response to M. tuberculosis is unknown. Methods: We assessed expression of glutamine pathway genes in M. tuberculosis-infected macrophages and blood transcriptomic profiles of individuals with latent M. tuberculosis infection or tuberculosis. Subsequently, we studied the effect of blocking glutaminolysis on M. tuberculosis-induced cytokines. Finally, we examined whether polymorphisms in genes involved in the glutamine pathway influence M. tuberculosis-induced cytokines in a cohort of 500 individuals. Results: Glutamine pathway genes were differentially expressed in infected macrophages and patients with tuberculosis. Human peripheral blood mononuclear cells stimulated with M. tuberculosis displayed decreased cytokine (ie, interleukin 1β, interferon γ, and interleukin 17) responses when medium was devoid of glutamine. Specific inhibitors of the glutamine pathway led to decreased cytokine responses, especially T-cell cytokines (ie, interferon γ, interleukin 17, and interleukin 22). Finally, genetic polymorphisms in glutamine metabolism genes (including GLS2, SLC1A5, and SLC7A5) influenced ex vivo cytokine responses to M. tuberculosis, especially for T-cell cytokines. Conclusions: Cellular glutamine metabolism is implicated in effective host responses against M. tuberculosis. Targeting immunometabolism may represent new strategies for tuberculosis prevention and/or treatment.
MeSH term(s)	Cells, Cultured ; Cytokines/metabolism ; Gene Expression Profiling ; Glutamine/metabolism ; Humans ; Latent Tuberculosis/immunology ; Latent Tuberculosis/metabolism ; Leukocytes, Mononuclear/immunology ; Leukocytes, Mononuclear/metabolism ; Macrophages/metabolism ; Mycobacterium tuberculosis/physiology ; Polymorphism, Genetic ; Tuberculosis/immunology ; Tuberculosis/metabolism
Chemical Substances	Cytokines ; Glutamine (0RH81L854J)
Language	English
Publishing date	2018-12-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiy709
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Article ; Online: Metformin enhances anti-mycobacterial responses by educating CD8+ T-cell immunometabolic circuits.

Nature communications

2020 Volume 11, Issue 1, Page(s) 5225

Abstract: Patients with type 2 diabetes (T2D) have a lower risk of Mycobacterium tuberculosis infection, progression from infection to tuberculosis (TB) disease, TB morality and TB recurrence, when being treated with metformin. However, a detailed mechanistic ... ...

Abstract	Patients with type 2 diabetes (T2D) have a lower risk of Mycobacterium tuberculosis infection, progression from infection to tuberculosis (TB) disease, TB morality and TB recurrence, when being treated with metformin. However, a detailed mechanistic understanding of these protective effects is lacking. Here, we use mass cytometry to show that metformin treatment expands a population of memory-like antigen-inexperienced CD8
MeSH term(s)	Animals ; BCG Vaccine/administration & dosage ; BCG Vaccine/immunology ; CD8-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/immunology ; Diabetes Mellitus, Type 2/metabolism ; Female ; Guinea Pigs ; Humans ; Hypoglycemic Agents/administration & dosage ; Male ; Metformin/administration & dosage ; Mice ; Mycobacterium tuberculosis/drug effects ; Mycobacterium tuberculosis/immunology ; Mycobacterium tuberculosis/physiology ; Tuberculosis/etiology ; Tuberculosis/immunology ; Tuberculosis/microbiology ; Tuberculosis/prevention & control
Chemical Substances	BCG Vaccine ; Hypoglycemic Agents ; Metformin (9100L32L2N)
Language	English
Publishing date	2020-10-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-020-19095-z
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Article ; Online: The effect of hyperglycaemia on in vitro cytokine production and macrophage infection with Mycobacterium tuberculosis.

Lachmandas, Ekta / Vrieling, Frank / Wilson, Louis G / Joosten, Simone A / Netea, Mihai G / Ottenhoff, Tom H / van Crevel, Reinout

PloS one

2015 Volume 10, Issue 2, Page(s) e0117941

Abstract: Type 2 diabetes mellitus is an established risk factor for tuberculosis but the underlying mechanisms are largely unknown. We examined the effects of hyperglycaemia, a hallmark of diabetes, on the cytokine response to and macrophage infection with ... ...

Abstract	Type 2 diabetes mellitus is an established risk factor for tuberculosis but the underlying mechanisms are largely unknown. We examined the effects of hyperglycaemia, a hallmark of diabetes, on the cytokine response to and macrophage infection with Mycobacterium tuberculosis. Increasing in vitro glucose concentrations from 5 to 25 mmol/L had marginal effects on cytokine production following stimulation of peripheral blood mononuclear cells (PBMCs) with M. tuberculosis lysate, LPS or Candida albicans, while 40 mmol/L glucose increased production of TNF-α, IL-1β, IL-6 and IL-10, but not of IFN-γ, IL-17A and IL-22. Macrophage differentiation under hyperglycaemic conditions of 25 mmol/L glucose was also associated with increased cytokine production upon stimulation with M. tuberculosis lysate and LPS but in infection experiments no differences in M. tuberculosis killing or outgrowth was observed. The phagocytic capacity of these hyperglycaemic macrophages also remained unaltered. The fact that only very high glucose concentrations were able to significantly influence cytokine production by macrophages suggests that hyperglycaemia alone cannot fully explain the increased susceptibility of diabetes mellitus patients to tuberculosis.
MeSH term(s)	Candida albicans/immunology ; Cell Differentiation/immunology ; Diabetes Mellitus, Type 2/immunology ; Diabetes Mellitus, Type 2/microbiology ; Humans ; Hyperglycemia/immunology ; Hyperglycemia/microbiology ; Interferon-gamma/immunology ; Interleukins/immunology ; Leukocytes, Mononuclear/immunology ; Leukocytes, Mononuclear/microbiology ; Lipopolysaccharides/immunology ; Macrophages/immunology ; Macrophages/microbiology ; Middle Aged ; Mycobacterium tuberculosis/immunology ; Tuberculosis/immunology ; Tuberculosis/microbiology ; Tumor Necrosis Factor-alpha/immunology
Chemical Substances	Interleukins ; Lipopolysaccharides ; Tumor Necrosis Factor-alpha ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0117941
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Diabetes Mellitus and Increased Tuberculosis Susceptibility: The Role of Short-Chain Fatty Acids.

Lachmandas, Ekta / van den Heuvel, Corina N A M / Damen, Michelle S M A / Cleophas, Maartje C P / Netea, Mihai G / van Crevel, Reinout

Journal of diabetes research

2015 Volume 2016, Page(s) 6014631

Abstract: Type 2 diabetes mellitus confers a threefold increased risk for tuberculosis, but the underlying immunological mechanisms are still largely unknown. Possible mediators of this increased susceptibility are short-chain fatty acids, levels of which have ... ...

Abstract	Type 2 diabetes mellitus confers a threefold increased risk for tuberculosis, but the underlying immunological mechanisms are still largely unknown. Possible mediators of this increased susceptibility are short-chain fatty acids, levels of which have been shown to be altered in individuals with diabetes. We examined the influence of physiological concentrations of butyrate on cytokine responses to Mycobacterium tuberculosis (Mtb) in human peripheral blood mononuclear cells (PBMCs). Butyrate decreased Mtb-induced proinflammatory cytokine responses, while it increased production of IL-10. This anti-inflammatory effect was independent of butyrate's well-characterised inhibition of HDAC activity and was not accompanied by changes in Toll-like receptor signalling pathways, the eicosanoid pathway, or cellular metabolism. In contrast blocking IL-10 activity reversed the effects of butyrate on Mtb-induced inflammation. Alteration of the gut microbiota, thereby increasing butyrate concentrations, can reduce insulin resistance and obesity, but further studies are needed to determine how this affects susceptibility to tuberculosis.
MeSH term(s)	Butyrates/pharmacology ; Cells, Cultured ; Cytokines/immunology ; Diabetes Complications/immunology ; Diabetes Complications/microbiology ; Host-Pathogen Interactions ; Humans ; Inflammation Mediators/immunology ; Leukocytes, Mononuclear/drug effects ; Leukocytes, Mononuclear/immunology ; Leukocytes, Mononuclear/microbiology ; Mycobacterium tuberculosis/immunology ; Signal Transduction/drug effects ; Time Factors ; Tuberculosis/immunology ; Tuberculosis/microbiology
Chemical Substances	Butyrates ; Cytokines ; Inflammation Mediators
Language	English
Publishing date	2015-12-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2711897-6
ISSN	2314-6753 ; 2314-6745
ISSN (online)	2314-6753
ISSN	2314-6745
DOI	10.1155/2016/6014631
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Article ; Online: Microbial stimulation of different Toll-like receptor signalling pathways induces diverse metabolic programmes in human monocytes.

Lachmandas, Ekta / Boutens, Lily / Ratter, Jacqueline M / Hijmans, Anneke / Hooiveld, Guido J / Joosten, Leo A B / Rodenburg, Richard J / Fransen, Jack A M / Houtkooper, Riekelt H / van Crevel, Reinout / Netea, Mihai G / Stienstra, Rinke

Nature microbiology

2016 Volume 2, Page(s) 16246

Abstract: Microbial stimuli such as lipopolysaccharide (LPS) induce robust metabolic rewiring in immune cells known as the Warburg effect. It is unknown whether this increase in glycolysis and decrease in oxidative phosphorylation (OXPHOS) is a general ... ...

Abstract	Microbial stimuli such as lipopolysaccharide (LPS) induce robust metabolic rewiring in immune cells known as the Warburg effect. It is unknown whether this increase in glycolysis and decrease in oxidative phosphorylation (OXPHOS) is a general characteristic of monocytes that have encountered a pathogen. Using CD14
Language	English
Publishing date	2016-12-19
Publishing country	England
Document type	Journal Article
ISSN	2058-5276
ISSN (online)	2058-5276
DOI	10.1038/nmicrobiol.2016.246
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Article ; Online: Metformin enhances anti-mycobacterial responses by educating CD8+ T-cell immunometabolic circuits

Nature Communications, Vol 11, Iss 1, Pp 1-

2020 Volume 15

Abstract: Metformin is an anti-diabetic drug that has shown promise to reduce M. tuberculosis susceptibility. Here the authors show that this effect is a result of metformin-mediated activation of anti-mycobacterial memory-like antigen-inexperienced CD8+CXCR3+ T ... ...

Abstract	Metformin is an anti-diabetic drug that has shown promise to reduce M. tuberculosis susceptibility. Here the authors show that this effect is a result of metformin-mediated activation of anti-mycobacterial memory-like antigen-inexperienced CD8+CXCR3+ T cells, an effect that also boosts response to BCG vaccination.
Keywords	Science ; Q
Language	English
Publishing date	2020-10-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The effect of hyperglycaemia on in vitro cytokine production and macrophage infection with Mycobacterium tuberculosis.

Ekta Lachmandas / Frank Vrieling / Louis G Wilson / Simone A Joosten / Mihai G Netea / Tom H Ottenhoff / Reinout van Crevel

PLoS ONE, Vol 10, Iss 2, p e

2015 Volume 0117941

Abstract	Type 2 diabetes mellitus is an established risk factor for tuberculosis but the underlying mechanisms are largely unknown. We examined the effects of hyperglycaemia, a hallmark of diabetes, on the cytokine response to and macrophage infection with Mycobacterium tuberculosis. Increasing in vitro glucose concentrations from 5 to 25 mmol/L had marginal effects on cytokine production following stimulation of peripheral blood mononuclear cells (PBMCs) with M. tuberculosis lysate, LPS or Candida albicans, while 40 mmol/L glucose increased production of TNF-α, IL-1β, IL-6 and IL-10, but not of IFN-γ, IL-17A and IL-22. Macrophage differentiation under hyperglycaemic conditions of 25 mmol/L glucose was also associated with increased cytokine production upon stimulation with M. tuberculosis lysate and LPS but in infection experiments no differences in M. tuberculosis killing or outgrowth was observed. The phagocytic capacity of these hyperglycaemic macrophages also remained unaltered. The fact that only very high glucose concentrations were able to significantly influence cytokine production by macrophages suggests that hyperglycaemia alone cannot fully explain the increased susceptibility of diabetes mellitus patients to tuberculosis.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2015-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Metformin Alters Human Host Responses to Mycobacterium tuberculosis in Healthy Subjects.

Lachmandas, Ekta / Eckold, Clare / Böhme, Julia / Koeken, Valerie A C M / Marzuki, Mardiana Binte / Blok, Bastiaan / Arts, Rob J W / Chen, Jinmiao / Teng, Karen W W / Ratter, Jacqueline / Smolders, Elise J / Van den Heuvel, Corina / Stienstra, Rinke / Dockrell, Hazel M / Newell, Evan / Netea, Mihai G / Singhal, Amit / Cliff, Jacqueline M / Van Crevel, Reinout

The Journal of infectious diseases

2019 Volume 220, Issue 1, Page(s) 139–150

Abstract: Background: Metformin, the most widely administered diabetes drug, has been proposed as a candidate adjunctive host-directed therapy for tuberculosis, but little is known about its effects on human host responses to Mycobacterium tuberculosis.: ... ...

Abstract	Background: Metformin, the most widely administered diabetes drug, has been proposed as a candidate adjunctive host-directed therapy for tuberculosis, but little is known about its effects on human host responses to Mycobacterium tuberculosis. Methods: We investigated in vitro and in vivo effects of metformin in humans. Results: Metformin added to peripheral blood mononuclear cells from healthy volunteers enhanced in vitro cellular metabolism while inhibiting the mammalian target of rapamycin targets p70S6K and 4EBP1, with decreased cytokine production and cellular proliferation and increased phagocytosis activity. Metformin administered to healthy human volunteers led to significant downregulation of genes involved in oxidative phosphorylation, mammalian target of rapamycin signaling, and type I interferon response pathways, particularly following stimulation with M. tuberculosis, and upregulation of genes involved in phagocytosis and reactive oxygen species production was increased. These in vivo effects were accompanied by a metformin-induced shift in myeloid cells from classical to nonclassical monocytes. At a functional level, metformin lowered ex vivo production of tumor necrosis factor α, interferon γ, and interleukin 1β but increased phagocytosis activity and reactive oxygen species production. Conclusion: Metformin has a range of potentially beneficial effects on cellular metabolism, immune function, and gene transcription involved in innate host responses to M. tuberculosis.
MeSH term(s)	Cell Proliferation/drug effects ; Down-Regulation/drug effects ; Healthy Volunteers ; Host-Pathogen Interactions/drug effects ; Humans ; Hypoglycemic Agents/pharmacology ; Leukocytes, Mononuclear/drug effects ; Leukocytes, Mononuclear/microbiology ; Metformin/pharmacology ; Monocytes/drug effects ; Monocytes/metabolism ; Mycobacterium tuberculosis/pathogenicity ; Myeloid Cells/drug effects ; Myeloid Cells/metabolism ; Phagocytosis/drug effects ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects ; Tuberculosis/metabolism ; Tuberculosis/microbiology ; Up-Regulation/drug effects
Chemical Substances	Hypoglycemic Agents ; Reactive Oxygen Species ; Metformin (9100L32L2N)
Language	English
Publishing date	2019-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiz064
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Article ; Online: Correction to: Rewiring of glucose metabolism defines trained immunity induced by oxidized low-density lipoprotein.

Keating, Samuel T / Groh, Laszlo / Thiem, Kathrin / Bekkering, Siroon / Li, Yang / Matzaraki, Vasiliki / van der Heijden, Charlotte D C C / van Puffelen, Jelmer H / Lachmandas, Ekta / Jansen, Trees / Oosting, Marije / de Bree, L Charlotte J / Koeken, Valerie A C M / Moorlag, Simone J C F M / Mourits, Vera P / van Diepen, Janna / Stienstra, Rinke / Novakovic, Boris / Stunnenberg, Hendrik G /

van Crevel, Reinout / Joosten, Leo A B / Netea, Mihai G / Riksen, Niels P

Journal of molecular medicine (Berlin, Germany)

2019 Volume 98, Issue 7, Page(s) 1051

Abstract: The correct name of the 17th Author is presented in this paper. ...

Abstract	The correct name of the 17th Author is presented in this paper.
Language	English
Publishing date	2019-10-03
Publishing country	Germany
Document type	Published Erratum
ZDB-ID	1223802-8
ISSN	1432-1440 ; 0946-2716
ISSN (online)	1432-1440
ISSN	0946-2716
DOI	10.1007/s00109-020-01939-2
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