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Cell Metab. 2017 Jul 5;26(1):71-93. doi: 10.1016/j.cmet.2017.06.018.

Inflammasomes on the Crossroads of Innate Immune Recognition and Metabolic Control.

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Institute of Innate Immunity, University Hospitals Bonn, 53127 Bonn, Germany.
Institute of Innate Immunity, University Hospitals Bonn, 53127 Bonn, Germany; Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA; German Center of Neurodegenerative Diseases (DZNE), 53127 Bonn, Germany; Centre for Molecular Inflammation Research (CEMIR), Norwegian University of Science and Technology, 7491 Trondheim, Norway. Electronic address:


Inflammasomes are protein complexes formed upon encounter of microbial or damage-associated stimuli. The main output of inflammasome assembly is activation of caspase-1, a protease involved in both pro-inflammatory and host-protective responses. Defined bacterial or viral ligands have been identified for the inflammasome-forming receptors AIM2, NLRP1, and NLRC4. The signals activating other inflammasomes, NLRP3, NLRP6, and pyrin, are less well understood. Recent studies implicated several low-molecular-weight compounds traditionally linked to metabolism, not immunity, in modulation of inflammasome signaling. Furthermore, genetic, pharmacological, or pathogen-mediated interference with energy metabolism also affects inflammasome activation. Here we review the findings on how microbial- and host-derived metabolites regulate activation of the NLRP3 and NLRP6 inflammasomes. We discuss the different models of how glycolysis and mitochondrial metabolism control the NLRP3 inflammasome. Finally, we summarize the findings on metabolic control of pyrin and point to open questions to be addressed to broaden our understanding of metabolism-inflammasome interactions.


NLRP3; NLRP6; glycolysis; gut microbiome; immunometabolism; inflammasome; innate immunity; mitochondria; pyrin; tricarboxylic acid cycle

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