Document Detail


Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1β in type 2 diabetes.
MedLine Citation:
PMID:  20835230     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Interleukin 1β (IL-1β) is an important inflammatory mediator of type 2 diabetes. Here we show that oligomers of islet amyloid polypeptide (IAPP), a protein that forms amyloid deposits in the pancreas during type 2 diabetes, triggered the NLRP3 inflammasome and generated mature IL-1β. One therapy for type 2 diabetes, glyburide, suppressed IAPP-mediated IL-1β production in vitro. Processing of IL-1β initiated by IAPP first required priming, a process that involved glucose metabolism and was facilitated by minimally oxidized low-density lipoprotein. Finally, mice transgenic for human IAPP had more IL-1β in pancreatic islets, which localized together with amyloid and macrophages. Our findings identify previously unknown mechanisms in the pathogenesis of type 2 diabetes and treatment of pathology caused by IAPP.
Authors:
Seth L Masters; Aisling Dunne; Shoba L Subramanian; Rebecca L Hull; Gillian M Tannahill; Fiona A Sharp; Christine Becker; Luigi Franchi; Eiji Yoshihara; Zhe Chen; Niamh Mullooly; Lisa A Mielke; James Harris; Rebecca C Coll; Kingston H G Mills; K Hun Mok; Philip Newsholme; Gabriel Nuñez; Junji Yodoi; Steven E Kahn; Ed C Lavelle; Luke A J O'Neill
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-09-12
Journal Detail:
Title:  Nature immunology     Volume:  11     ISSN:  1529-2916     ISO Abbreviation:  Nat. Immunol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-21     Completed Date:  2010-11-03     Revised Date:  2011-07-28    
Medline Journal Info:
Nlm Unique ID:  100941354     Medline TA:  Nat Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  897-904     Citation Subset:  IM    
Affiliation:
Immunology Research Centre, School of Biochemistry and Immunology, Trinity College, Dublin, Ireland. smasters@tcd.ie
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MeSH Terms
Descriptor/Qualifier:
Amyloid / metabolism*
Animals
Carrier Proteins / antagonists & inhibitors,  genetics,  metabolism*
Cells, Cultured
Dendritic Cells / immunology,  metabolism
Diabetes Mellitus, Type 2 / immunology*,  metabolism
Glyburide / pharmacology
Humans
Hypoglycemic Agents / pharmacology
Interleukin-1beta / metabolism*
Islet Amyloid Polypeptide
Islets of Langerhans / metabolism
Macrophages / immunology,  metabolism
Mice
Mice, Inbred C57BL
Mice, Transgenic
Rats
Grant Support
ID/Acronym/Agency:
AI063331/AI/NIAID NIH HHS; DK-75998/DK/NIDDK NIH HHS; R01 DK075998-03/DK/NIDDK NIH HHS; R01 DK075998-04/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Amyloid; 0/Carrier Proteins; 0/Hypoglycemic Agents; 0/Interleukin-1beta; 0/Islet Amyloid Polypeptide; 0/NLRP3 protein, human; 10238-21-8/Glyburide
Comments/Corrections
Comment In:
Nat Immunol. 2010 Oct;11(10):881-3   [PMID:  20856216 ]
Cell Metab. 2010 Nov 3;12(5):427-8   [PMID:  21035753 ]
Nat Rev Immunol. 2010 Nov;10(11):748   [PMID:  21080610 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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