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  • Mice, Inbred C57BL  (165)
  • Astronomy
  • Chemistry
  • Condensed Matter: Electronic Properties, etc.
  • Nature Publishing Group (NPG)  (168)
  • 2010-2014  (168)
  • 1955-1959
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  • 11
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    Vascular endothelial growth factor B controls endothelial fatty acid uptake (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-03-17
    Description: The vascular endothelial growth factors (VEGFs) are major angiogenic regulators and are involved in several aspects of endothelial cell physiology. However, the detailed role of VEGF-B in blood vessel function has remained unclear. Here we show that VEGF-B has an unexpected role in endothelial targeting of lipids to peripheral tissues. Dietary lipids present in circulation have to be transported through the vascular endothelium to be metabolized by tissue cells, a mechanism that is poorly understood. Bioinformatic analysis showed that Vegfb was tightly co-expressed with nuclear-encoded mitochondrial genes across a large variety of physiological conditions in mice, pointing to a role for VEGF-B in metabolism. VEGF-B specifically controlled endothelial uptake of fatty acids via transcriptional regulation of vascular fatty acid transport proteins. As a consequence, Vegfb(-/-) mice showed less uptake and accumulation of lipids in muscle, heart and brown adipose tissue, and instead shunted lipids to white adipose tissue. This regulation was mediated by VEGF receptor 1 and neuropilin 1 expressed by the endothelium. The co-expression of VEGF-B and mitochondrial proteins introduces a novel regulatory mechanism, whereby endothelial lipid uptake and mitochondrial lipid use are tightly coordinated. The involvement of VEGF-B in lipid uptake may open up the possibility for novel strategies to modulate pathological lipid accumulation in diabetes, obesity and cardiovascular diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagberg, Carolina E -- Falkevall, Annelie -- Wang, Xun -- Larsson, Erik -- Huusko, Jenni -- Nilsson, Ingrid -- van Meeteren, Laurens A -- Samen, Erik -- Lu, Li -- Vanwildemeersch, Maarten -- Klar, Joakim -- Genove, Guillem -- Pietras, Kristian -- Stone-Elander, Sharon -- Claesson-Welsh, Lena -- Yla-Herttuala, Seppo -- Lindahl, Per -- Eriksson, Ulf -- England -- Nature. 2010 Apr 8;464(7290):917-21. doi: 10.1038/nature08945. Epub 2010 Mar 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tissue Biology Group, Division of Matrix Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20228789" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/metabolism ; Animals ; Biological Transport ; Cell Line ; Cell Nucleus/genetics ; Cells, Cultured ; Endothelium/cytology/*metabolism ; Fatty Acid Transport Proteins/genetics ; Fatty Acids/*metabolism ; Gene Expression Regulation ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/genetics/metabolism ; Mitochondrial Proteins/genetics/metabolism ; Muscles/metabolism ; Myocardium/metabolism ; Neuropilin-1/genetics/metabolism ; Oligonucleotide Array Sequence Analysis ; Organ Specificity ; Signal Transduction ; Transcription, Genetic ; Vascular Endothelial Growth Factor B/deficiency/genetics/*metabolism ; Vascular Endothelial Growth Factor Receptor-1/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 12
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    Gut inflammation provides a respiratory electron acceptor for Salmonella (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-09-25
    Description: Salmonella enterica serotype Typhimurium (S. Typhimurium) causes acute gut inflammation by using its virulence factors to invade the intestinal epithelium and survive in mucosal macrophages. The inflammatory response enhances the transmission success of S. Typhimurium by promoting its outgrowth in the gut lumen through unknown mechanisms. Here we show that reactive oxygen species generated during inflammation react with endogenous, luminal sulphur compounds (thiosulphate) to form a new respiratory electron acceptor, tetrathionate. The genes conferring the ability to use tetrathionate as an electron acceptor produce a growth advantage for S. Typhimurium over the competing microbiota in the lumen of the inflamed gut. We conclude that S. Typhimurium virulence factors induce host-driven production of a new electron acceptor that allows the pathogen to use respiration to compete with fermenting gut microbes. Thus the ability to trigger intestinal inflammation is crucial for the biology of this diarrhoeal pathogen.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2946174/" 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/PMC2946174/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Winter, Sebastian E -- Thiennimitr, Parameth -- Winter, Maria G -- Butler, Brian P -- Huseby, Douglas L -- Crawford, Robert W -- Russell, Joseph M -- Bevins, Charles L -- Adams, L Garry -- Tsolis, Renee M -- Roth, John R -- Baumler, Andreas J -- AI040124/AI/NIAID NIH HHS/ -- AI044170/AI/NIAID NIH HHS/ -- AI073120/AI/NIAID NIH HHS/ -- AI076246/AI/NIAID NIH HHS/ -- AI088122/AI/NIAID NIH HHS/ -- R21 AI088122/AI/NIAID NIH HHS/ -- R21 AI088122-01/AI/NIAID NIH HHS/ -- R21 AI088122-02/AI/NIAID NIH HHS/ -- England -- Nature. 2010 Sep 23;467(7314):426-9. doi: 10.1038/nature09415.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, One Shields Avenue, Davis, California 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20864996" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Respiration ; Colitis/metabolism/microbiology ; Electron Transport ; *Electrons ; Female ; Gastrointestinal Tract/metabolism/*microbiology/*pathology ; Inflammation/metabolism/microbiology/pathology ; Intestinal Mucosa/metabolism/microbiology/pathology ; Mice ; Mice, Inbred C57BL ; Reactive Oxygen Species/metabolism ; Salmonella typhimurium/growth & development/*metabolism ; Tetrathionic Acid/metabolism ; Thiosulfates/metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 13
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    Maintenance of muscle stem-cell quiescence by microRNA-489 (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-02-24
    Description: Among the key properties that distinguish adult mammalian stem cells from their more differentiated progeny is the ability of stem cells to remain in a quiescent state for prolonged periods of time. However, the molecular pathways for the maintenance of stem-cell quiescence remain elusive. Here we use adult mouse muscle stem cells (satellite cells) as a model system and show that the microRNA (miRNA) pathway is essential for the maintenance of the quiescent state. Satellite cells that lack a functional miRNA pathway spontaneously exit quiescence and enter the cell cycle. We identified quiescence-specific miRNAs in the satellite-cell lineage by microarray analysis. Among these, miRNA-489 (miR-489) is highly expressed in quiescent satellite cells and is quickly downregulated during satellite-cell activation. Further analysis revealed that miR-489 functions as a regulator of satellite-cell quiescence, as it post-transcriptionally suppresses the oncogene Dek, the protein product of which localizes to the more differentiated daughter cell during asymmetric division of satellite cells and promotes the transient proliferative expansion of myogenic progenitors. Our results provide evidence of the miRNA pathway in general, and of a specific miRNA, miR-489, in actively maintaining the quiescent state of an adult stem-cell population.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3292200/" 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/PMC3292200/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheung, Tom H -- Quach, Navaline L -- Charville, Gregory W -- Liu, Ling -- Park, Lidia -- Edalati, Abdolhossein -- Yoo, Bryan -- Hoang, Phuong -- Rando, Thomas A -- DP1 OD000392/OD/NIH HHS/ -- DP1 OD000392-05/OD/NIH HHS/ -- F30 AG035521/AG/NIA NIH HHS/ -- P01 AG036695/AG/NIA NIH HHS/ -- P01 AG036695-01A1/AG/NIA NIH HHS/ -- P01AG036695/AG/NIA NIH HHS/ -- R01 AG023806/AG/NIA NIH HHS/ -- R01 AG023806-05/AG/NIA NIH HHS/ -- R01 AR056849/AR/NIAMS NIH HHS/ -- R01 AR056849-03/AR/NIAMS NIH HHS/ -- R01 AR062185/AR/NIAMS NIH HHS/ -- R01 AR062185-01/AR/NIAMS NIH HHS/ -- R01AG23806/AG/NIA NIH HHS/ -- R37 AG023806/AG/NIA NIH HHS/ -- England -- Nature. 2012 Feb 23;482(7386):524-8. doi: 10.1038/nature10834.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22358842" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects/*genetics ; Cell Differentiation/drug effects ; Cell Lineage/drug effects ; Cell Survival/drug effects/genetics ; DEAD-box RNA Helicases/genetics/metabolism ; DNA-Binding Proteins/genetics ; *Gene Expression Regulation/drug effects ; Gene Knockdown Techniques ; Mice ; Mice, Inbred C57BL ; MicroRNAs/*genetics ; Myoblasts/*cytology/drug effects/*metabolism ; Oligonucleotide Array Sequence Analysis ; Oncogene Proteins/genetics ; Ribonuclease III/genetics/metabolism ; Satellite Cells, Skeletal Muscle/cytology/drug effects/metabolism ; Tamoxifen/pharmacology ; Transcription, Genetic/drug effects
    Print ISSN: 0028-0836
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  • 14
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    Regulation of myeloid leukaemia by the cell-fate determinant Musashi (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-20
    Description: Chronic myelogenous leukaemia (CML) can progress from a slow growing chronic phase to an aggressive blast crisis phase, but the molecular basis of this transition remains poorly understood. Here we have used mouse models of CML to show that disease progression is regulated by the Musashi-Numb signalling axis. Specifically, we find that the chronic phase is marked by high levels of Numb expression whereas the blast crisis phase has low levels of Numb expression, and that ectopic expression of Numb promotes differentiation and impairs advanced-phase disease in vivo. As a possible explanation for the decreased levels of Numb in the blast crisis phase, we show that NUP98-HOXA9, an oncogene associated with blast crisis CML, can trigger expression of the RNA-binding protein Musashi2 (Msi2), which in turn represses Numb. Notably, loss of Msi2 restores Numb expression and significantly impairs the development and propagation of blast crisis CML in vitro and in vivo. Finally we show that Msi2 expression is not only highly upregulated during human CML progression but is also an early indicator of poorer prognosis. These data show that the Musashi-Numb pathway can control the differentiation of CML cells, and raise the possibility that targeting this pathway may provide a new strategy for the therapy of aggressive leukaemias.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2918284/" 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/PMC2918284/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Takahiro -- Kwon, Hyog Young -- Zimdahl, Bryan -- Congdon, Kendra L -- Blum, Jordan -- Lento, William E -- Zhao, Chen -- Lagoo, Anand -- Gerrard, Gareth -- Foroni, Letizia -- Goldman, John -- Goh, Harriet -- Kim, Soo-Hyun -- Kim, Dong-Wook -- Chuah, Charles -- Oehler, Vivian G -- Radich, Jerald P -- Jordan, Craig T -- Reya, Tannishtha -- AI067798/AI/NIAID NIH HHS/ -- CA122206/CA/NCI NIH HHS/ -- CA140371/CA/NCI NIH HHS/ -- CA18029/CA/NCI NIH HHS/ -- DK072234/DK/NIDDK NIH HHS/ -- DK63031/DK/NIDDK NIH HHS/ -- DP1 CA174422/CA/NCI NIH HHS/ -- DP1 OD006430/OD/NIH HHS/ -- DP1 OD006430-01/OD/NIH HHS/ -- DP1 OD006430-02/OD/NIH HHS/ -- DP1OD006430/OD/NIH HHS/ -- HL097767/HL/NHLBI NIH HHS/ -- P01 CA018029/CA/NCI NIH HHS/ -- R01 CA140371/CA/NCI NIH HHS/ -- R01 DK063031/DK/NIDDK NIH HHS/ -- R01 DK063031-01/DK/NIDDK NIH HHS/ -- R01 DK063031-01S1/DK/NIDDK NIH HHS/ -- R01 DK063031-02/DK/NIDDK NIH HHS/ -- R01 DK063031-03/DK/NIDDK NIH HHS/ -- R01 DK063031-04/DK/NIDDK NIH HHS/ -- R01 DK063031-05/DK/NIDDK NIH HHS/ -- R01 DK063031-06/DK/NIDDK NIH HHS/ -- R01 DK063031-07/DK/NIDDK NIH HHS/ -- R01 DK063031-07S1/DK/NIDDK NIH HHS/ -- R01 DK063031-08/DK/NIDDK NIH HHS/ -- R01 DK072234/DK/NIDDK NIH HHS/ -- R01 DK072234-01A1/DK/NIDDK NIH HHS/ -- R01 DK072234-02/DK/NIDDK NIH HHS/ -- R01 DK072234-03/DK/NIDDK NIH HHS/ -- R01 DK072234-04/DK/NIDDK NIH HHS/ -- R01 HL097767/HL/NHLBI NIH HHS/ -- R01 HL097767-01/HL/NHLBI NIH HHS/ -- R01 HL097767-02/HL/NHLBI NIH HHS/ -- T32 GM007184-33/GM/NIGMS NIH HHS/ -- U19 AI067798/AI/NIAID NIH HHS/ -- U19 AI067798-010006/AI/NIAID NIH HHS/ -- U19 AI067798-020006/AI/NIAID NIH HHS/ -- U19 AI067798-030006/AI/NIAID NIH HHS/ -- U19 AI067798-040006/AI/NIAID NIH HHS/ -- U19 AI067798-050006/AI/NIAID NIH HHS/ -- England -- Nature. 2010 Aug 5;466(7307):765-8. doi: 10.1038/nature09171. Epub 2010 Jul 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20639863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blast Crisis/genetics/metabolism/pathology ; *Cell Differentiation/genetics ; Disease Progression ; Fusion Proteins, bcr-abl/genetics/metabolism ; Gene Expression Regulation, Neoplastic ; Homeodomain Proteins/genetics/metabolism ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics/*metabolism/*pathology ; Membrane Proteins/biosynthesis/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/biosynthesis/genetics/metabolism ; Nuclear Pore Complex Proteins/genetics/metabolism ; Oncogene Proteins, Fusion/genetics/metabolism ; Prognosis ; RNA-Binding Proteins/biosynthesis/genetics/*metabolism ; Receptor, Notch1/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/metabolism ; Up-Regulation
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 15
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    Lkb1 regulates quiescence and metabolic homeostasis of haematopoietic stem cells (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-03
    Description: The capacity to fine-tune cellular bioenergetics with the demands of stem-cell maintenance and regeneration is central to normal development and ageing, and to organismal survival during periods of acute stress. How energy metabolism and stem-cell homeostatic processes are coordinated is not well understood. Lkb1 acts as an evolutionarily conserved regulator of cellular energy metabolism in eukaryotic cells and functions as the major upstream kinase to phosphorylate AMP-activated protein kinase (AMPK) and 12 other AMPK-related kinases. Whether Lkb1 regulates stem-cell maintenance remains unknown. Here we show that Lkb1 has an essential role in haematopoietic stem cell (HSC) homeostasis. We demonstrate that ablation of Lkb1 in adult mice results in severe pancytopenia and subsequent lethality. Loss of Lkb1 leads to impaired survival and escape from quiescence of HSCs, resulting in exhaustion of the HSC pool and a marked reduction of HSC repopulating potential in vivo. Lkb1 deletion has an impact on cell proliferation in HSCs, but not on more committed compartments, pointing to context-specific functions for Lkb1 in haematopoiesis. The adverse impact of Lkb1 deletion on haematopoiesis was predominantly cell-autonomous and mTOR complex 1 (mTORC1)-independent, and involves multiple mechanisms converging on mitochondrial apoptosis and possibly downregulation of PGC-1 coactivators and their transcriptional network, which have critical roles in mitochondrial biogenesis and function. Thus, Lkb1 serves as an essential regulator of HSCs and haematopoiesis, and more generally, points to the critical importance of coupling energy metabolism and stem-cell homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058342/" 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/PMC3058342/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gan, Boyi -- Hu, Jian -- Jiang, Shan -- Liu, Yingchun -- Sahin, Ergun -- Zhuang, Li -- Fletcher-Sananikone, Eliot -- Colla, Simona -- Wang, Y Alan -- Chin, Lynda -- Depinho, Ronald A -- 01CA141508/CA/NCI NIH HHS/ -- R21 CA135057/CA/NCI NIH HHS/ -- R21 CA135057-01/CA/NCI NIH HHS/ -- R21CA135057/CA/NCI NIH HHS/ -- U01 CA141508/CA/NCI NIH HHS/ -- U01 CA141508-01/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 2;468(7324):701-4. doi: 10.1038/nature09595.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21124456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Cycle/*physiology ; Cell Proliferation ; Cell Survival ; *Energy Metabolism ; Female ; Gene Deletion ; Hematopoiesis ; Hematopoietic Stem Cells/*cytology/*metabolism/pathology ; *Homeostasis ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria/metabolism/pathology ; Multiprotein Complexes ; Pancytopenia/genetics ; Phenotype ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Proteins/metabolism ; Survival Analysis ; TOR Serine-Threonine Kinases ; Transcription Factors/metabolism
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  • 16
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    Subcapsular sinus macrophages prevent CNS invasion on peripheral infection with a neurotropic virus (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-06-26
    Description: Lymph nodes (LNs) capture microorganisms that breach the body's external barriers and enter draining lymphatics, limiting the systemic spread of pathogens. Recent work has shown that CD11b(+)CD169(+) macrophages, which populate the subcapsular sinus (SCS) of LNs, are critical for the clearance of viruses from the lymph and for initiating antiviral humoral immune responses. Here we show, using vesicular stomatitis virus (VSV), a relative of rabies virus transmitted by insect bites, that SCS macrophages perform a third vital function: they prevent lymph-borne neurotropic viruses from infecting the central nervous system (CNS). On local depletion of LN macrophages, about 60% of mice developed ascending paralysis and died 7-10 days after subcutaneous infection with a small dose of VSV, whereas macrophage-sufficient animals remained asymptomatic and cleared the virus. VSV gained access to the nervous system through peripheral nerves in macrophage-depleted LNs. In contrast, within macrophage-sufficient LNs VSV replicated preferentially in SCS macrophages but not in adjacent nerves. Removal of SCS macrophages did not compromise adaptive immune responses against VSV, but decreased type I interferon (IFN-I) production within infected LNs. VSV-infected macrophages recruited IFN-I-producing plasmacytoid dendritic cells to the SCS and in addition were a major source of IFN-I themselves. Experiments in bone marrow chimaeric mice revealed that IFN-I must act on both haematopoietic and stromal compartments, including the intranodal nerves, to prevent lethal infection with VSV. These results identify SCS macrophages as crucial gatekeepers to the CNS that prevent fatal viral invasion of the nervous system on peripheral infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892812/" 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/PMC2892812/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iannacone, Matteo -- Moseman, E Ashley -- Tonti, Elena -- Bosurgi, Lidia -- Junt, Tobias -- Henrickson, Sarah E -- Whelan, Sean P -- Guidotti, Luca G -- von Andrian, Ulrich H -- AI069259/AI/NIAID NIH HHS/ -- AI072252/AI/NIAID NIH HHS/ -- AI078897/AI/NIAID NIH HHS/ -- AR42689/AR/NIAMS NIH HHS/ -- P01 AI078897/AI/NIAID NIH HHS/ -- P01 AI078897-01/AI/NIAID NIH HHS/ -- P01 CA071932/CA/NCI NIH HHS/ -- P01 CA071932-12S29003/CA/NCI NIH HHS/ -- R01 AI069259/AI/NIAID NIH HHS/ -- R01 AI069259-06/AI/NIAID NIH HHS/ -- R01 AI072252/AI/NIAID NIH HHS/ -- R01 AI072252-04/AI/NIAID NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Jun 24;465(7301):1079-83. doi: 10.1038/nature09118.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Disease Institute and Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA. Matteo_Iannacone@hms.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20577213" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Central Nervous System/cytology/*immunology/*virology ; Dendritic Cells/immunology ; Injections ; Interferon Type I/immunology ; Lymph Nodes/cytology/*immunology/innervation/*virology ; Macrophages/*immunology/virology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Paralysis/complications/virology ; Peripheral Nerves/virology ; Receptor, Interferon alpha-beta/deficiency ; Rhabdoviridae Infections/complications/*immunology/virology ; Survival Rate ; Vesicular stomatitis Indiana virus/immunology/pathogenicity/physiology ; Vesicular stomatitis New Jersey virus/immunology/pathogenicity/physiology ; Vesiculovirus/*immunology/pathogenicity/physiology
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  • 17
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    NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-30
    Description: The inflammatory nature of atherosclerosis is well established but the agent(s) that incite inflammation in the artery wall remain largely unknown. Germ-free animals are susceptible to atherosclerosis, suggesting that endogenous substances initiate the inflammation. Mature atherosclerotic lesions contain macroscopic deposits of cholesterol crystals in the necrotic core, but their appearance late in atherogenesis had been thought to disqualify them as primary inflammatory stimuli. However, using a new microscopic technique, we revealed that minute cholesterol crystals are present in early diet-induced atherosclerotic lesions and that their appearance in mice coincides with the first appearance of inflammatory cells. Other crystalline substances can induce inflammation by stimulating the caspase-1-activating NLRP3 (NALP3 or cryopyrin) inflammasome, which results in cleavage and secretion of interleukin (IL)-1 family cytokines. Here we show that cholesterol crystals activate the NLRP3 inflammasome in phagocytes in vitro in a process that involves phagolysosomal damage. Similarly, when injected intraperitoneally, cholesterol crystals induce acute inflammation, which is impaired in mice deficient in components of the NLRP3 inflammasome, cathepsin B, cathepsin L or IL-1 molecules. Moreover, when mice deficient in low-density lipoprotein receptor (LDLR) were bone-marrow transplanted with NLRP3-deficient, ASC (also known as PYCARD)-deficient or IL-1alpha/beta-deficient bone marrow and fed on a high-cholesterol diet, they had markedly decreased early atherosclerosis and inflammasome-dependent IL-18 levels. Minimally modified LDL can lead to cholesterol crystallization concomitant with NLRP3 inflammasome priming and activation in macrophages. Although there is the possibility that oxidized LDL activates the NLRP3 inflammasome in vivo, our results demonstrate that crystalline cholesterol acts as an endogenous danger signal and its deposition in arteries or elsewhere is an early cause rather than a late consequence of inflammation. These findings provide new insights into the pathogenesis of atherosclerosis and indicate new potential molecular targets for the therapy of this disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2946640/" 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/PMC2946640/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duewell, Peter -- Kono, Hajime -- Rayner, Katey J -- Sirois, Cherilyn M -- Vladimer, Gregory -- Bauernfeind, Franz G -- Abela, George S -- Franchi, Luigi -- Nunez, Gabriel -- Schnurr, Max -- Espevik, Terje -- Lien, Egil -- Fitzgerald, Katherine A -- Rock, Kenneth L -- Moore, Kathryn J -- Wright, Samuel D -- Hornung, Veit -- Latz, Eicke -- R01 AI075318/AI/NIAID NIH HHS/ -- R01 AI083713/AI/NIAID NIH HHS/ -- R01 AI083713-01/AI/NIAID NIH HHS/ -- R01 HL093262/HL/NHLBI NIH HHS/ -- R01 HL093262-01A1/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Apr 29;464(7293):1357-61. doi: 10.1038/nature08938.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20428172" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis Regulatory Proteins ; Atherosclerosis/chemically induced/*metabolism/*pathology ; Bone Marrow Transplantation ; Carrier Proteins/genetics/*metabolism ; Cathepsin B/metabolism ; Cathepsin L/metabolism ; Cholesterol/*chemistry/*metabolism/pharmacology ; Crystallization ; Cytoskeletal Proteins/deficiency ; Diet, Atherogenic ; Female ; Humans ; Inflammation/chemically induced/metabolism/pathology ; Interleukin-1/deficiency ; Interleukin-18/metabolism ; Lysosomes/drug effects/pathology ; Mice ; Mice, Inbred C57BL ; Peritoneal Cavity/pathology ; Phagocytes/drug effects/pathology/physiology ; Receptors, LDL/deficiency ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    In vivo imaging of Treg cells providing immune privilege to the haematopoietic stem-cell niche (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-06-10
    Description: Stem cells reside in a specialized regulatory microenvironment or niche, where they receive appropriate support for maintaining self-renewal and multi-lineage differentiation capacity. The niche may also protect stem cells from environmental insults including cytotoxic chemotherapy and perhaps pathogenic immunity. The testis, hair follicle and placenta are all sites of residence for stem cells and are immune-suppressive environments, called immune-privileged sites, where multiple mechanisms cooperate to prevent immune attack, even enabling prolonged survival of foreign allografts without immunosuppression. We sought to determine if somatic stem-cell niches more broadly are immune-privileged sites by examining the haematopoietic stem/progenitor cell (HSPC) niche in the bone marrow, a site where immune reactivity exists. We observed persistence of HSPCs from allogeneic donor mice (allo-HSPCs) in non-irradiated recipient mice for 30 days without immunosuppression with the same survival frequency compared to syngeneic HSPCs. These HSPCs were lost after the depletion of FoxP3 regulatory T (T(reg)) cells. High-resolution in vivo imaging over time demonstrated marked co-localization of HSPCs with T(reg) cells that accumulated on the endosteal surface in the calvarial and trabecular bone marrow. T(reg) cells seem to participate in creating a localized zone where HSPCs reside and where T(reg) cells are necessary for allo-HSPC persistence. In addition to processes supporting stem-cell function, the niche will provide a relative sanctuary from immune attack.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725645/" 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/PMC3725645/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujisaki, Joji -- Wu, Juwell -- Carlson, Alicia L -- Silberstein, Lev -- Putheti, Prabhakar -- Larocca, Rafael -- Gao, Wenda -- Saito, Toshiki I -- Lo Celso, Cristina -- Tsuyuzaki, Hitoshi -- Sato, Tatsuyuki -- Cote, Daniel -- Sykes, Megan -- Strom, Terry B -- Scadden, David T -- Lin, Charles P -- AI041521/AI/NIAID NIH HHS/ -- CA111519/CA/NCI NIH HHS/ -- HL097748/HL/NHLBI NIH HHS/ -- HL97794/HL/NHLBI NIH HHS/ -- P01 AI041521/AI/NIAID NIH HHS/ -- P01 AI073748/AI/NIAID NIH HHS/ -- P01 CA111519/CA/NCI NIH HHS/ -- P01 CA111519-05/CA/NCI NIH HHS/ -- R01 HL097748/HL/NHLBI NIH HHS/ -- R01 HL097748-02/HL/NHLBI NIH HHS/ -- R01 HL097794/HL/NHLBI NIH HHS/ -- R01 HL097794-02/HL/NHLBI NIH HHS/ -- England -- Nature. 2011 Jun 8;474(7350):216-9. doi: 10.1038/nature10160.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Advanced Microscopy Program, Center for Systems Biology and Wellman Center for Photomedicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA. jfujisaki@partners.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21654805" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival/immunology ; Cells, Cultured ; Forkhead Transcription Factors/metabolism ; Graft Survival/*immunology ; Hematopoietic Stem Cells/cytology/*immunology ; Humans ; *Imaging, Three-Dimensional ; Interleukin-10/deficiency/genetics/immunology/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Stem Cell Niche/cytology/*immunology ; T-Lymphocytes, Regulatory/*immunology/metabolism ; Time Factors ; Transplantation, Homologous/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Acquisition of a multifunctional IgA+ plasma cell phenotype in the gut (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-12-14
    Description: The largest mucosal surface in the body is in the gastrointestinal tract, a location that is heavily colonized by microbes that are normally harmless. A key mechanism required for maintaining a homeostatic balance between this microbial burden and the lymphocytes that densely populate the gastrointestinal tract is the production and transepithelial transport of poly-reactive IgA (ref. 1). Within the mucosal tissues, B cells respond to cytokines, sometimes in the absence of T-cell help, undergo class switch recombination of their immunoglobulin receptor to IgA, and differentiate to become plasma cells. However, IgA-secreting plasma cells probably have additional attributes that are needed for coping with the tremendous bacterial load in the gastrointestinal tract. Here we report that mouse IgA(+) plasma cells also produce the antimicrobial mediators tumour-necrosis factor-alpha (TNF-alpha) and inducible nitric oxide synthase (iNOS), and express many molecules that are commonly associated with monocyte/granulocytic cell types. The development of iNOS-producing IgA(+) plasma cells can be recapitulated in vitro in the presence of gut stroma, and the acquisition of this multifunctional phenotype in vivo and in vitro relies on microbial co-stimulation. Deletion of TNF-alpha and iNOS in B-lineage cells resulted in a reduction in IgA production, altered diversification of the gut microbiota and poor clearance of a gut-tropic pathogen. These findings reveal a novel adaptation to maintaining homeostasis in the gut, and extend the repertoire of protective responses exhibited by some B-lineage cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3487691/" 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/PMC3487691/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fritz, Jorg H -- Rojas, Olga Lucia -- Simard, Nathalie -- McCarthy, Douglas D -- Hapfelmeier, Siegfried -- Rubino, Stephen -- Robertson, Susan J -- Larijani, Mani -- Gosselin, Jean -- Ivanov, Ivaylo I -- Martin, Alberto -- Casellas, Rafael -- Philpott, Dana J -- Girardin, Stephen E -- McCoy, Kathy D -- Macpherson, Andrew J -- Paige, Christopher J -- Gommerman, Jennifer L -- 67157-3/Canadian Institutes of Health Research/Canada -- 89783-2/Canadian Institutes of Health Research/Canada -- MOP 114972/Canadian Institutes of Health Research/Canada -- MOP 67157/Canadian Institutes of Health Research/Canada -- MOP 89783/Canadian Institutes of Health Research/Canada -- MOP 9862/Canadian Institutes of Health Research/Canada -- R00 DK085329/DK/NIDDK NIH HHS/ -- R00 DK085329-02/DK/NIDDK NIH HHS/ -- Z01 AR041148-03/Intramural NIH HHS/ -- ZIA AR041148-08/Intramural NIH HHS/ -- England -- Nature. 2011 Dec 11;481(7380):199-203. doi: 10.1038/nature10698.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Toronto, Toronto M5S 1A8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22158124" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/cytology ; Cell Lineage ; Cells, Cultured ; Chimera/immunology ; Citrobacter rodentium/immunology ; Coculture Techniques ; Female ; Germ-Free Life ; Granulocytes/cytology/metabolism ; Immunity, Innate/immunology ; Immunoglobulin A/biosynthesis/*immunology ; Intestinal Mucosa/cytology/immunology ; Intestine, Small/*cytology/*immunology/microbiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Monocytes/cytology/metabolism ; Nitric Oxide Synthase Type II/biosynthesis/deficiency/metabolism ; Phenotype ; Plasma Cells/*cytology/*immunology/metabolism ; Spleen/cytology ; Stromal Cells/cytology ; Tumor Necrosis Factor-alpha/biosynthesis/deficiency/immunology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Adenoma-linked barrier defects and microbial products drive IL-23/IL-17-mediated tumour growth (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-10-05
    Description: Approximately 2% of colorectal cancer is linked to pre-existing inflammation known as colitis-associated cancer, but most develops in patients without underlying inflammatory bowel disease. Colorectal cancer often follows a genetic pathway whereby loss of the adenomatous polyposis coli (APC) tumour suppressor and activation of beta-catenin are followed by mutations in K-Ras, PIK3CA and TP53, as the tumour emerges and progresses. Curiously, however, 'inflammatory signature' genes characteristic of colitis-associated cancer are also upregulated in colorectal cancer. Further, like most solid tumours, colorectal cancer exhibits immune/inflammatory infiltrates, referred to as 'tumour-elicited inflammation'. Although infiltrating CD4(+) T(H)1 cells and CD8(+) cytotoxic T cells constitute a positive prognostic sign in colorectal cancer, myeloid cells and T-helper interleukin (IL)-17-producing (T(H)17) cells promote tumorigenesis, and a 'T(H)17 expression signature' in stage I/II colorectal cancer is associated with a drastic decrease in disease-free survival. Despite its pathogenic importance, the mechanisms responsible for the appearance of tumour-elicited inflammation are poorly understood. Many epithelial cancers develop proximally to microbial communities, which are physically separated from immune cells by an epithelial barrier. We investigated mechanisms responsible for tumour-elicited inflammation in a mouse model of colorectal tumorigenesis, which, like human colorectal cancer, exhibits upregulation of IL-23 and IL-17. Here we show that IL-23 signalling promotes tumour growth and progression, and development of a tumoural IL-17 response. IL-23 is mainly produced by tumour-associated myeloid cells that are likely to be activated by microbial products, which penetrate the tumours but not adjacent tissue. Both early and late colorectal neoplasms exhibit defective expression of several barrier proteins. We propose that barrier deterioration induced by colorectal-cancer-initiating genetic lesions results in adenoma invasion by microbial products that trigger tumour-elicited inflammation, which in turn drives tumour growth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601659/" 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/PMC3601659/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grivennikov, Sergei I -- Wang, Kepeng -- Mucida, Daniel -- Stewart, C Andrew -- Schnabl, Bernd -- Jauch, Dominik -- Taniguchi, Koji -- Yu, Guann-Yi -- Osterreicher, Christoph H -- Hung, Kenneth E -- Datz, Christian -- Feng, Ying -- Fearon, Eric R -- Oukka, Mohamed -- Tessarollo, Lino -- Coppola, Vincenzo -- Yarovinsky, Felix -- Cheroutre, Hilde -- Eckmann, Lars -- Trinchieri, Giorgio -- Karin, Michael -- AI043477/AI/NIAID NIH HHS/ -- DK035108/DK/NIDDK NIH HHS/ -- DK080506/DK/NIDDK NIH HHS/ -- K08 DK081830/DK/NIDDK NIH HHS/ -- K99 DK088589/DK/NIDDK NIH HHS/ -- K99-DK088589/DK/NIDDK NIH HHS/ -- R01 AA020703/AA/NIAAA NIH HHS/ -- R01 AI043477/AI/NIAID NIH HHS/ -- R01 AI050265/AI/NIAID NIH HHS/ -- R01 CA082223/CA/NCI NIH HHS/ -- R01CA082223/CA/NCI NIH HHS/ -- England -- Nature. 2012 Nov 8;491(7423):254-8. doi: 10.1038/nature11465.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla, California 92093-0723, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23034650" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/genetics/immunology/*microbiology/*pathology ; Animals ; Bacteria/metabolism/pathogenicity ; Cell Division ; Cell Transformation, Neoplastic/*pathology ; Colitis/complications ; Colorectal Neoplasms/genetics/immunology/*microbiology/*pathology ; Disease Models, Animal ; Disease-Free Survival ; Genes, APC ; Humans ; Inflammation/genetics/immunology/microbiology/pathology ; Interleukin-17/genetics/*immunology ; Interleukin-23/deficiency/genetics/*immunology ; Mice ; Mice, Inbred C57BL ; Myeloid Cells/immunology/metabolism ; Myeloid Differentiation Factor 88/immunology/metabolism ; Signal Transduction ; Toll-Like Receptors/immunology/metabolism ; Tumor Microenvironment ; beta Catenin/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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