Inflammasomes on the Crossroads of Innate Immune Recognition and Metabolic Control

Autor: Eicke Latz, Tomasz Próchnicki
Jazyk: angličtina
Rok vydání: 2017
Předmět:
0301 basic medicine
Physiology
immunology [NLR Family
Pyrin Domain-Containing 3 Protein]

Inflammasomes
metabolism [NLR Family
Pyrin Domain-Containing 3 Protein]

NLRP12 protein
human

Mitochondrion
Biology
metabolism [Bacteria]
Pyrin domain
03 medical and health sciences
AIM2
NLRC4
immunology [Intracellular Signaling Peptides and Proteins]
ddc:570
immunology [Bacterial Infections]
NLR Family
Pyrin Domain-Containing 3 Protein

medicine
Animals
Humans
Molecular Biology
microbiology [Mitochondria]
NLRP6
Innate immune system
Bacteria
NLRP1
Intracellular Signaling Peptides and Proteins
Inflammasome
Bacterial Infections
Cell Biology
immunology [Mitochondria]
metabolism [Mitochondria]
Immunity
Innate

Mitochondria
Cell biology
Gastrointestinal Microbiome
immunology [Inflammasomes]
NLRP6 protein
human

030104 developmental biology
immunology [Bacteria]
metabolism [Bacterial Infections]
Host-Pathogen Interactions
Glycolysis
metabolism [Inflammasomes]
metabolism [Intracellular Signaling Peptides and Proteins]
Metabolic Networks and Pathways
medicine.drug
Zdroj: Cell metabolism 26(1), 71-93 (2017). doi:10.1016/j.cmet.2017.06.018
DOI: 10.1016/j.cmet.2017.06.018
Popis: 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.
Databáze: OpenAIRE