Metformin Alters Human Host Responses to Mycobacterium tuberculosis in Healthy Subjects
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 eff...
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| Vydáno v: | The Journal of infectious diseases Ročník 220; číslo 1; s. 139 - 150 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Oxford University Press
05.06.2019
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| ISSN: | 0022-1899, 1537-6613, 1537-6613 |
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| Abstract | 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.
Metformin has shown beneficial effects in a murine model of tuberculosis. Using in-vitro and in-vivo studies we show that metformin has beneficial effects on cellular metabolism, immune function and genetranscription involved in innate host responses to M. tuberculosis in humans. |
|---|---|
| AbstractList | 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.
Metformin has shown beneficial effects in a murine model of tuberculosis. Using in-vitro and in-vivo studies we show that metformin has beneficial effects on cellular metabolism, immune function and genetranscription involved in innate host responses to M. tuberculosis in humans. 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. We investigated in vitro and in vivo effects of metformin in humans. 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. Metformin has a range of potentially beneficial effects on cellular metabolism, immune function, and gene transcription involved in innate host responses to M. tuberculosis. 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.BACKGROUNDMetformin, 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.We investigated in vitro and in vivo effects of metformin in humans.METHODSWe investigated in vitro and in vivo effects of metformin in humans.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.RESULTSMetformin 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.Metformin has a range of potentially beneficial effects on cellular metabolism, immune function, and gene transcription involved in innate host responses to M. tuberculosis.CONCLUSIONMetformin has a range of potentially beneficial effects on cellular metabolism, immune function, and gene transcription involved in innate host responses to M. tuberculosis. |
| Author | Lachmandas, Ekta Newell, Evan Netea, Mihai G Ratter, Jacqueline Blok, Bastiaan Van den Heuvel, Corina Arts, Rob J W Marzuki, Mardiana Binte Eckold, Clare Teng, Karen W W Smolders, Elise J Van Crevel, Reinout Böhme, Julia Singhal, Amit Cliff, Jacqueline M Koeken, Valerie A C M Chen, Jinmiao Stienstra, Rinke Dockrell, Hazel M |
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| Keywords | gene transcription host-directed therapy Metformin antimycobacterial mechanisms tuberculosis |
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Background
Metformin, the most widely administered diabetes drug, has been proposed as a candidate adjunctive host-directed therapy for tuberculosis,... Metformin, the most widely administered diabetes drug, has been proposed as a candidate adjunctive host-directed therapy for tuberculosis, but little is known... |
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| SubjectTerms | 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 |
| Title | Metformin Alters Human Host Responses to Mycobacterium tuberculosis in Healthy Subjects |
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