| Glucose activation of islets of Langerhans up-regulates Toll-like receptor 5: possible mechanism of protection. | |
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MedLine Citation:
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PMID: 21985371 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Toll-like receptors are pattern-recognition receptors of the innate immune system that are activated during viral, bacterial or other infections, as well as during disease progression of type 1 and type 2 diabetes. Toll-like receptor 5 (TLR-5) specifically recognizes bacterial infection through binding of flagellin from pathogenic bacteria such as Salmonella and Listeria species. We have found that the expression of TLR5 is up-regulated by glucose activation of isolated islets of Langerhans, in contrast to other investigated TLRs (TLR-2, -3, -4, -6 and -9. Stimulation of islets with 10 mm glucose increased the levels of TLR5 mRNA 10-fold (P=0·03) and the TLR-5 protein levels twofold (P=0·04). Furthermore, the protein level of downstream signalling molecule myeloid differentiation primary response gene 88 (MyD88) increased 1·6-fold (P=0·01). Activation of TLR-5 in islets lead to a marked reduction of both stimulated and basal secretion of insulin, as well as an increase in production of nitric oxide, proinflammatory cytokines, anti-inflammatory heat-shock protein and major histocompatibility complex (MHC) class I transporter. We observe no effects of TLR-5 activation on islet survival. We suggest that this regulation by TLR-5 might be beneficial during serious infection such as sepsis by limiting the activity of beta cells during peaks of insulin demand to counteract beta cell damage. |
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Authors:
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C Weile; K Josefsen; K Buschard |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Clinical and experimental immunology Volume: 166 ISSN: 1365-2249 ISO Abbreviation: Clin. Exp. Immunol. Publication Date: 2011 Nov |
Date Detail:
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Created Date: 2011-10-11 Completed Date: 2011-11-28 Revised Date: 2011-11-30 |
Medline Journal Info:
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Nlm Unique ID: 0057202 Medline TA: Clin Exp Immunol Country: England |
Other Details:
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Languages: eng Pagination: 251-7 Citation Subset: IM |
Copyright Information:
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© 2011 The Authors. Clinical and Experimental Immunology © 2011 British Society for Immunology. |
Affiliation:
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The Bartholin Institute, Rigshospitalet, Copenhagen, Denmark. cweile@yahoo.dk |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Line, Tumor Cytokines / biosynthesis Glucose / metabolism* Heat-Shock Proteins / biosynthesis Inflammation / immunology, metabolism Insulin / secretion Islets of Langerhans / metabolism* Major Histocompatibility Complex / drug effects Male Mice Mice, Inbred BALB C Myeloid Differentiation Factor 88 / biosynthesis, metabolism Nitric Oxide / biosynthesis RNA, Messenger / genetics, metabolism Rats Rats, Inbred Lew Reverse Transcriptase Polymerase Chain Reaction Toll-Like Receptor 5 / genetics, immunology, metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Heat-Shock Proteins; 0/Insulin; 0/Myd88 protein, mouse; 0/Myeloid Differentiation Factor 88; 0/RNA, Messenger; 0/Toll-Like Receptor 5; 10102-43-9/Nitric Oxide; 50-99-7/Glucose |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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