Document Detail


Linking lipid metabolism to the innate immune response in macrophages through sterol regulatory element binding protein-1a.
MedLine Citation:
PMID:  21531336     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We show that mice with a targeted deficiency in the gene encoding the lipogenic transcription factor SREBP-1a are resistant to endotoxic shock and systemic inflammatory response syndrome induced by cecal ligation and puncture (CLP). When macrophages from the mutant mice were challenged with bacterial lipopolysaccharide, they failed to activate lipogenesis as well as two hallmark inflammasome functions, activation of caspase-1 and secretion of IL-1β. We show that SREBP-1a activates not only genes required for lipogenesis in macrophages but also the gene encoding Nlrp1a, which is a core inflammasome component. Thus, SREBP-1a links lipid metabolism to the innate immune response, which supports our hypothesis that SREBPs evolved to regulate cellular reactions to external challenges that range from nutrient limitation and hypoxia to toxins and pathogens.
Authors:
Seung-Soon Im; Leyla Yousef; Christoph Blaschitz; Janet Z Liu; Robert A Edwards; Stephen G Young; Manuela Raffatellu; Timothy F Osborne
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Cell metabolism     Volume:  13     ISSN:  1932-7420     ISO Abbreviation:  Cell Metab.     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-05-02     Completed Date:  2011-09-05     Revised Date:  2012-05-07    
Medline Journal Info:
Nlm Unique ID:  101233170     Medline TA:  Cell Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  540-9     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
Affiliation:
Metabolic Signaling and Disease Program, Sanford-Burnham Medical Research Institute, Orlando, FL 32827, USA.
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MeSH Terms
Descriptor/Qualifier:
Adaptor Proteins, Signal Transducing / antagonists & inhibitors,  genetics,  metabolism*
Animals
Apoptosis Regulatory Proteins / antagonists & inhibitors,  genetics,  metabolism*
Blotting, Western
Bone Marrow
Caspase 1 / metabolism
Cytokines / metabolism
Enzyme Activation / drug effects
Enzyme-Linked Immunosorbent Assay
Immunity, Innate*
Inflammasomes
Interleukin-1beta / secretion
Lipid Metabolism*
Lipopolysaccharides / pharmacology
Macrophages / cytology,  immunology*,  metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
RNA, Messenger / genetics
RNA, Small Interfering / genetics
Reverse Transcriptase Polymerase Chain Reaction
Salmonella Infections / immunology*,  metabolism,  pathology
Salmonella typhimurium / immunology
Sterol Regulatory Element Binding Protein 1 / physiology*
Grant Support
ID/Acronym/Agency:
AI083619/AI/NIAID NIH HHS; AI083663/AI/NIAID NIH HHS; HL48044/HL/NHLBI NIH HHS; R01 AI083663-01A1/AI/NIAID NIH HHS; R01 HL048044-17/HL/NHLBI NIH HHS; R01 HL048044-19/HL/NHLBI NIH HHS; R21 AI083619-01/AI/NIAID NIH HHS; T32 AI60573/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Apoptosis Regulatory Proteins; 0/Cytokines; 0/Inflammasomes; 0/Interleukin-1beta; 0/Lipopolysaccharides; 0/NALP1 protein, mouse; 0/RNA, Messenger; 0/RNA, Small Interfering; 0/Srebf1 protein, mouse; 0/Sterol Regulatory Element Binding Protein 1; EC 3.4.22.36/Caspase 1
Comments/Corrections
Comment In:
Nat Rev Immunol. 2011 Jun;11(6):368-9   [PMID:  21610734 ]

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