Document Detail


(1,3)-beta-glucans activate both dectin-1 and NLRP3 inflammasome in human macrophages.
MedLine Citation:
PMID:  20421639     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
beta-Glucans are naturally occurring polysaccharides that are the major cell wall components of fungi. Recognition of beta-glucans is mediated through a membrane-bound pattern recognition receptor called dectin-1, and gene knock-out studies have shown that dectin-1 plays an important role in antifungal immune response in vivo. In this report, we have studied the effect of large particulate (1,3)-beta-glucans, including curdlan, glucan from baker's yeast, paramylon, and zymosan, on inflammatory response in human macrophages. We show that beta-glucans activate the transcription of the proinflammatory cytokine IL-1beta through a dectin-1-dependent pathway in human macrophages. Moreover, dectin-1 receptor associated Syk tyrosine kinase was essential for beta-glucan induced IL-1beta mRNA expression. In contrast to LPS, beta-glucans also strongly activated the secretion of IL-1beta. This beta-glucan triggered IL-1beta release was abolished by cytochalasin D, an inhibitor of phagocytosis, demonstrating that cytosolic recognition of beta-glucans is required for IL-1beta response in human macrophages. RNA interference-mediated gene knockdown experiments demonstrated that cytoplasmic NLRP3 inflammasome is essential for beta-glucan-induced IL-1beta secretion. Moreover, our results suggest that beta-glucan-induced NLRP3 inflammasome activation is dependent on the dectin-1/Syk signaling pathway. Furthermore, our results suggest that the lysosomal cathepsin B protease, the formation of reactive oxygen species, and the efflux of potassium are needed for beta-glucan-induced NLRP3 inflammasome activation. In conclusion, our results show that beta-glucans are recognized by membrane-associated dectin-1 and cytoplasmic NLRP3 inflammasome resulting in IL-1beta gene transcription and IL-1beta secretion in human macrophages, respectively.
Authors:
P?ivi Kankkunen; Laura Teiril?; Johanna Rintahaka; Harri Alenius; Henrik Wolff; Sampsa Matikainen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-04-26
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  184     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-20     Completed Date:  2010-06-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  6335-42     Citation Subset:  AIM; IM    
Affiliation:
Unit of Excellence for Immunotoxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
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MeSH Terms
Descriptor/Qualifier:
Blotting, Western
Carrier Proteins / immunology*,  metabolism
Enzyme-Linked Immunosorbent Assay
Fungal Proteins / immunology,  metabolism
Gene Expression
Gene Expression Regulation / immunology
Humans
Interleukin-1beta / biosynthesis,  immunology
Macrophage Activation / immunology*
Macrophages / immunology*,  metabolism
Membrane Proteins / immunology*,  metabolism
Nerve Tissue Proteins / immunology*,  metabolism
RNA Interference
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction / immunology
beta-Glucans / immunology*,  metabolism
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/Fungal Proteins; 0/Interleukin-1beta; 0/Membrane Proteins; 0/NLRP3 protein, human; 0/Nerve Tissue Proteins; 0/beta-Glucans; 0/dectin 1

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