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      AMP-Activated Protein Kinase and Host Defense against Infection

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          Abstract

          5′-AMP-activated protein kinase (AMPK) plays diverse roles in various physiological and pathological conditions. AMPK is involved in energy metabolism, which is perturbed by infectious stimuli. Indeed, various pathogens modulate AMPK activity, which affects host defenses against infection. In some viral infections, including hepatitis B and C viral infections, AMPK activation is beneficial, but in others such as dengue virus, Ebola virus, and human cytomegaloviral infections, AMPK plays a detrimental role. AMPK-targeting agents or small molecules enhance the antiviral response and contribute to the control of microbial and parasitic infections. In addition, this review focuses on the double-edged role of AMPK in innate and adaptive immune responses to infection. Understanding how AMPK regulates host defenses will enable development of more effective host-directed therapeutic strategies against infectious diseases.

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          Calmodulin-dependent protein kinase kinase-beta is an alternative upstream kinase for AMP-activated protein kinase.

          Simon A. Hawley, David Pan, Kirsty Mustard … (2005)
          The AMP-activated protein kinase (AMPK) is a critical regulator of energy balance at both the cellular and whole-body levels. Two upstream kinases have been reported to activate AMPK in cell-free assays, i.e., the tumor suppressor LKB1 and calmodulin-dependent protein kinase kinase. However, evidence that this is physiologically relevant currently only exists for LKB1. We now report that there is a significant basal activity and phosphorylation of AMPK in LKB1-deficient cells that can be stimulated by Ca2+ ionophores, and studies using the CaMKK inhibitor STO-609 and isoform-specific siRNAs show that CaMKKbeta is required for this effect. CaMKKbeta also activates AMPK much more rapidly than CaMKKalpha in cell-free assays. K(+)-induced depolarization in rat cerebrocortical slices, which increases intracellular Ca2+ without disturbing cellular adenine nucleotide levels, activates AMPK, and this is blocked by STO-609. Our results suggest a potential Ca(2+)-dependent neuroprotective pathway involving phosphorylation and activation of AMPK by CaMKKbeta.
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            AMPK is a negative regulator of the Warburg effect and suppresses tumor growth in vivo.

            Brandon Faubert, Gino Boily, Said Izreig … (2013)
            AMPK is a metabolic sensor that helps maintain cellular energy homeostasis. Despite evidence linking AMPK with tumor suppressor functions, the role of AMPK in tumorigenesis and tumor metabolism is unknown. Here we show that AMPK negatively regulates aerobic glycolysis (the Warburg effect) in cancer cells and suppresses tumor growth in vivo. Genetic ablation of the α1 catalytic subunit of AMPK accelerates Myc-induced lymphomagenesis. Inactivation of AMPKα in both transformed and nontransformed cells promotes a metabolic shift to aerobic glycolysis, increased allocation of glucose carbon into lipids, and biomass accumulation. These metabolic effects require normoxic stabilization of the hypoxia-inducible factor-1α (HIF-1α), as silencing HIF-1α reverses the shift to aerobic glycolysis and the biosynthetic and proliferative advantages conferred by reduced AMPKα signaling. Together our findings suggest that AMPK activity opposes tumor development and that its loss fosters tumor progression in part by regulating cellular metabolic pathways that support cell growth and proliferation. Copyright © 2013 Elsevier Inc. All rights reserved.
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              The energy sensor AMPK regulates T cell metabolic adaptation and effector responses in vivo.

              Julianna Blagih, François Coulombe, Emma Vincent … (2015)
              Naive T cells undergo metabolic reprogramming to support the increased energetic and biosynthetic demands of effector T cell function. However, how nutrient availability influences T cell metabolism and function remains poorly understood. Here we report plasticity in effector T cell metabolism in response to changing nutrient availability. Activated T cells were found to possess a glucose-sensitive metabolic checkpoint controlled by the energy sensor AMP-activated protein kinase (AMPK) that regulated mRNA translation and glutamine-dependent mitochondrial metabolism to maintain T cell bioenergetics and viability. T cells lacking AMPKα1 displayed reduced mitochondrial bioenergetics and cellular ATP in response to glucose limitation in vitro or pathogenic challenge in vivo. Finally, we demonstrated that AMPKα1 is essential for T helper 1 (Th1) and Th17 cell development and primary T cell responses to viral and bacterial infections in vivo. Our data highlight AMPK-dependent regulation of metabolic homeostasis as a key regulator of T cell-mediated adaptive immunity. Copyright © 2015 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 06 November 2018
                Publication date Collection: November 2018
                Volume: 19
                Issue: 11
                Electronic Location Identifier: 3495
                Affiliations
                [1 ]Department of Microbiology, Chungnam National University School of Medicine, Daejeon 35015, Korea; pst.ktz@ 123456gmail.com (P.S.); pcjlovesh6@ 123456naver.com (J.K.K.)
                [2 ]Infection Control Convergence Research Center, Chungnam National University School of Medicine, Daejeon 35015, Korea
                [3 ]Department of Medical Science, Chungnam National University School of Medicine, Daejeon 35015, Korea
                [4 ]Department of Infection Biology, Chungnam National University School of Medicine, Daejeon 35015, Korea; yjaemin0@ 123456cnu.ac.kr
                Author notes
                [* ]Correspondence: hayoungj@ 123456cnu.ac.kr ; Tel.: +82-42-580-8243; Fax: +82-42-585-3686
                Author information
                https://orcid.org/0000-0002-8332-024X
                Article
                Publisher ID: ijms-19-03495
                DOI: 10.3390/ijms19113495
                PMC ID: 6274990
                PubMed ID: 30404221
                SO-VID: 56ceb04a-06e6-4a0e-a2ef-44eb4c4a02bb
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 27 September 2018
                Date accepted : 05 November 2018
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: ampk,infection,mycobacteria,host defense
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: ampk, infection, mycobacteria, host defense

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