IL-33-induced metabolic reprogramming controls the differentiation of alternatively activated macrophages and the resolution of inflammation

Faas, Maria M.; Ipseiz, Natacha; Ackermann, Jochen A.; Culemann, Stephan; Grüneboom, Anika; Schröder, Fenja; Rothe, Tobias; Scholtysek, Carina; Eberhardt, Martin; Böttcher, Martin; Kirchner, Philipp; Stoll, Cornelia; Ekici, Arif B.; Fuchs, Maximilian; Kunz, Meik; Weigmann, Benno; Wirtz, Stefan; Lang, Roland; Hofmann, Joerg; Vera, Julio; Voehringer, David; Michelucci, Alessandro; Mougiakakos, Dimitrios; Uderhardt, Stefan; Schett, Georg; Krönke, Gerhard

doi:10.1016/j.immuni.2021.09.010

Cited by 85 publications

(77 citation statements)

References 51 publications

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“…Many cells achieve this by activating glucose transporters [ 19 , 20 ]. Additionally, metabolic reprogrammed cells exhibit an increase in glycolytic enzymes to promote further glycolysis [ 4 , 21 ]. Cells experiencing metabolic reprogramming utilize HIF-1α and c-Myc transcription factors, master inducers of glycolysis, to upregulate glucose transporters and glycolytic enzymes ( Figure 2 A) [ 15 ].…”

Section: Glycolysismentioning

confidence: 99%

Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Allen

Arjona

Santerre

et al. 2022

Viruses

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Metabolic reprogramming is a hallmark of cancer and has proven to be critical in viral infections. Metabolic reprogramming provides the cell with energy and biomass for large-scale biosynthesis. Based on studies of the cellular changes that contribute to metabolic reprogramming, seven main hallmarks can be identified: (1) increased glycolysis and lactic acid, (2) increased glutaminolysis, (3) increased pentose phosphate pathway, (4) mitochondrial changes, (5) increased lipid metabolism, (6) changes in amino acid metabolism, and (7) changes in other biosynthetic and bioenergetic pathways. Viruses depend on metabolic reprogramming to increase biomass to fuel viral genome replication and production of new virions. Viruses take advantage of the non-metabolic effects of metabolic reprogramming, creating an anti-apoptotic environment and evading the immune system. Other non-metabolic effects can negatively affect cellular function. Understanding the role metabolic reprogramming plays in viral pathogenesis may provide better therapeutic targets for antivirals.

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Section: Glycolysismentioning

confidence: 99%

Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Allen

Arjona

Santerre

et al. 2022

Viruses

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“…Among the acylation targets of succinate is gasdermin D, which when so modified, no longer supports pyroptosis ( Humphries et al., 2020 ). The inflammation-resolving effects of IL-33 have been traced to its promotion of increased production of itaconate ( Faas et al., 2021 ). Among the diverse effects of itaconate are inhibition of the NLRP3 inflammasome and activation of Nrf2 and ATF3, transcription factors with anti-inflammatory regulons ( Peace and O’Neill, 2022 ).…”

Section: Inflammation-regulating Metabolitesmentioning

confidence: 99%

Nonresolving inflammation redux

Nathan

2022

Immunity

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“…Targeting of specific populations as well as distinct pathway elements thus appears tempting for therapeutic purposes [ 272 ]. For example, local IL-1 administration might aid in the phenotypic priming of alternatively activated macrophages via activation of GATA-3, and timed local administration of platelets could also potentially aid in the shifting of inflammatory cell phenotypes [ 51 , 273 ]. Furthermore, the PAM3-based M2-phenotypic priming of macrophages was used in translational animal models to improve disease course in lupus and inflammatory colitis [ 274 , 275 ].…”

Section: Translational Findings and Immune Phenomics Of Covid-19mentioning

confidence: 99%

Immune Cell Plasticity in Inflammation: Insights into Description and Regulation of Immune Cell Phenotypes

Margraf

Perretti

2022

Cells

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Inflammation is a life-saving immune reaction occurring in response to invading pathogens. Nonetheless, inflammation can also occur in an uncontrolled, unrestricted manner, leading to chronic disease and organ damage. Mechanisms triggering an inflammatory response, hindering such a response, or leading to its resolution are well-studied but so far insufficiently elucidated with regard to precise therapeutic interventions. Notably, as an immune reaction evolves, requirements and environments for immune cells change, and thus cellular phenotypes adapt and shift, leading to the appearance of distinct cellular subpopulations with new functional features. In this article, we aim to highlight properties of, and overarching regulatory factors involved in, the occurrence of immune cell phenotypes with a special focus on neutrophils, macrophages and platelets. Additionally, we point out implications for both diagnostics and therapeutics in inflammation research.

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IL-33-induced metabolic reprogramming controls the differentiation of alternatively activated macrophages and the resolution of inflammation

Cited by 85 publications

References 51 publications

Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Nonresolving inflammation redux

Immune Cell Plasticity in Inflammation: Insights into Description and Regulation of Immune Cell Phenotypes

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