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  • 1
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    Syk kinase signalling couples to the Nlrp3 inflammasome for anti-fungal host defence (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-04-03
    Description: Fungal infections represent a serious threat, particularly in immunocompromised patients. Interleukin-1beta (IL-1beta) is a key pro-inflammatory factor in innate antifungal immunity. The mechanism by which the mammalian immune system regulates IL-1beta production after fungal recognition is unclear. Two signals are generally required for IL-1beta production: an NF-kappaB-dependent signal that induces the synthesis of pro-IL-1beta (p35), and a second signal that triggers proteolytic pro-IL-1beta processing to produce bioactive IL-1beta (p17) via Caspase-1-containing multiprotein complexes called inflammasomes. Here we demonstrate that the tyrosine kinase Syk, operating downstream of several immunoreceptor tyrosine-based activation motif (ITAM)-coupled fungal pattern recognition receptors, controls both pro-IL-1beta synthesis and inflammasome activation after cell stimulation with Candida albicans. Whereas Syk signalling for pro-IL-1beta synthesis selectively uses the Card9 pathway, inflammasome activation by the fungus involves reactive oxygen species production and potassium efflux. Genetic deletion or pharmalogical inhibition of Syk selectively abrogated inflammasome activation by C. albicans but not by inflammasome activators such as Salmonella typhimurium or the bacterial toxin nigericin. Nlrp3 (also known as NALP3) was identified as the critical NOD-like receptor family member that transduces the fungal recognition signal to the inflammasome adaptor Asc (Pycard) for Caspase-1 (Casp1) activation and pro-IL-1beta processing. Consistent with an essential role for Nlrp3 inflammasomes in antifungal immunity, we show that Nlrp3-deficient mice are hypersusceptible to Candida albicans infection. Thus, our results demonstrate the molecular basis for IL-1beta production after fungal infection and identify a crucial function for the Nlrp3 inflammasome in mammalian host defence in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gross, Olaf -- Poeck, Hendrik -- Bscheider, Michael -- Dostert, Catherine -- Hannesschlager, Nicole -- Endres, Stefan -- Hartmann, Gunther -- Tardivel, Aubry -- Schweighoffer, Edina -- Tybulewicz, Victor -- Mocsai, Attila -- Tschopp, Jurg -- Ruland, Jurgen -- MC_U117527252/Medical Research Council/United Kingdom -- England -- Nature. 2009 May 21;459(7245):433-6. doi: 10.1038/nature07965. Epub 2009 Apr 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉III. Medizinische Klinik, Klinikum rechts der Isar, Technische Universitat Munchen, Ismaninger Str. 22, 81675 Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19339971" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Candida albicans/*immunology/physiology ; Carrier Proteins/*immunology/*metabolism ; Caspase 1/metabolism ; Enzyme Activation ; Humans ; Inflammation/immunology ; Interleukin-1beta/biosynthesis/immunology ; Intracellular Signaling Peptides and Proteins/antagonists & ; inhibitors/deficiency/genetics/*metabolism ; Macrophages/metabolism ; Mice ; Monocytes/metabolism ; Nigericin/pharmacology ; Potassium/metabolism ; Protein-Tyrosine Kinases/antagonists & inhibitors/deficiency/genetics/*metabolism ; Reactive Oxygen Species/metabolism ; *Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    T cells dampen innate immune responses through inhibition of NLRP1 and NLRP3 inflammasomes (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-06-06
    Description: Inflammation is a protective attempt by the host to remove injurious stimuli and initiate the tissue healing process. The inflammatory response must be actively terminated, however, because failure to do so can result in 'bystander' damage to tissues and diseases such as arthritis or type-2 diabetes. Yet the mechanisms controlling excessive inflammatory responses are still poorly understood. Here we show that mouse effector and memory CD4(+) T cells abolish macrophage inflammasome-mediated caspase-1 activation and subsequent interleukin 1beta release in a cognate manner. Inflammasome inhibition is observed for all tested NLRP1 (commonly called NALP1) and NLRP3 (NALP3 or cryopyrin) activators, whereas NLRC4 (IPAF) inflammasome function and release of other inflammatory mediators such as CXCL2, interleukin 6 and tumour necrosis factor are not affected. Suppression of the NLRP3 inflammasome requires cell-to-cell contact and can be mimicked by macrophage stimulation with selected ligands of the tumour necrosis factor family, such as CD40L (also known as CD40LG). In a NLRP3-dependent peritonitis model, effector CD4(+) T cells are responsible for decreasing neutrophil recruitment in an antigen-dependent manner. Our findings reveal an unexpected mechanism of inflammasome inhibition, whereby effector and memory T cells suppress potentially damaging inflammation, yet leave the primary inflammatory response, crucial for the onset of immunity, intact.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guarda, Greta -- Dostert, Catherine -- Staehli, Francesco -- Cabalzar, Katrin -- Castillo, Rosa -- Tardivel, Aubry -- Schneider, Pascal -- Tschopp, Jurg -- England -- Nature. 2009 Jul 9;460(7252):269-73. doi: 10.1038/nature08100. Epub 2009 Jun 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, CH-1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19494813" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/*antagonists & inhibitors/metabolism ; Animals ; Antigens/immunology ; Apoptosis Regulatory Proteins/*antagonists & inhibitors/metabolism ; Bone Marrow Cells/cytology ; CD4-Positive T-Lymphocytes/*immunology ; Carrier Proteins/*antagonists & inhibitors/metabolism ; Caspase 1/metabolism ; Cells, Cultured ; Immunity, Innate/*immunology ; Immunologic Memory ; Inflammation/immunology/*metabolism/pathology ; Interleukin-1beta/immunology ; Ligands ; Macrophages/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neutrophils/immunology ; Peritoneal Cavity/cytology ; Tumor Necrosis Factors/immunology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Innate immune activation through Nalp3 inflammasome sensing of asbestos and silica (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-12
    Description: The inhalation of airborne pollutants, such as asbestos or silica, is linked to inflammation of the lung, fibrosis, and lung cancer. How the presence of pathogenic dust is recognized and how chronic inflammatory diseases are triggered are poorly understood. Here, we show that asbestos and silica are sensed by the Nalp3 inflammasome, whose subsequent activation leads to interleukin-1beta secretion. Inflammasome activation is triggered by reactive oxygen species, which are generated by a NADPH oxidase upon particle phagocytosis. (NADPH is the reduced form of nicotinamide adenine dinucleotide phosphate.) In a model of asbestos inhalation, Nalp3-/- mice showed diminished recruitment of inflammatory cells to the lungs, paralleled by lower cytokine production. Our findings implicate the Nalp3 inflammasome in particulate matter-related pulmonary diseases and support its role as a major proinflammatory "danger" receptor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2396588/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2396588/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dostert, Catherine -- Petrilli, Virginie -- Van Bruggen, Robin -- Steele, Chad -- Mossman, Brooke T -- Tschopp, Jurg -- P01 CA114047/CA/NCI NIH HHS/ -- P01 CA114047-01A10002/CA/NCI NIH HHS/ -- P01HL67004/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2008 May 2;320(5876):674-7. doi: 10.1126/science.1156995. Epub 2008 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, 1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403674" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asbestos/*immunology ; Carrier Proteins/*physiology ; Humans ; Immunity ; Inflammation/*immunology ; Inflammation Mediators/*physiology ; Interleukin-1beta/secretion ; Macrophages/immunology/secretion ; Mice ; Silicon Dioxide/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Activation of the NALP3 inflammasome is triggered by low intracellular potassium concentration (2007)
    Springer Nature
    Details
    Publication Date: 2007-06-29
    Print ISSN: 1350-9047
    Electronic ISSN: 1476-5403
    Topics: Biology , Medicine
    Published by Springer Nature
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