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  • 1
    Publication Date: 2014-01-28
    Description: Ancient genomic sequences have started to reveal the origin and the demographic impact of farmers from the Neolithic period spreading into Europe. The adoption of farming, stock breeding and sedentary societies during the Neolithic may have resulted in adaptive changes in genes associated with immunity and diet. However, the limited data available from earlier hunter-gatherers preclude an understanding of the selective processes associated with this crucial transition to agriculture in recent human evolution. Here we sequence an approximately 7,000-year-old Mesolithic skeleton discovered at the La Brana-Arintero site in Leon, Spain, to retrieve a complete pre-agricultural European human genome. Analysis of this genome in the context of other ancient samples suggests the existence of a common ancient genomic signature across western and central Eurasia from the Upper Paleolithic to the Mesolithic. The La Brana individual carries ancestral alleles in several skin pigmentation genes, suggesting that the light skin of modern Europeans was not yet ubiquitous in Mesolithic times. Moreover, we provide evidence that a significant number of derived, putatively adaptive variants associated with pathogen resistance in modern Europeans were already present in this hunter-gatherer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269527/" 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/PMC4269527/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olalde, Inigo -- Allentoft, Morten E -- Sanchez-Quinto, Federico -- Santpere, Gabriel -- Chiang, Charleston W K -- DeGiorgio, Michael -- Prado-Martinez, Javier -- Rodriguez, Juan Antonio -- Rasmussen, Simon -- Quilez, Javier -- Ramirez, Oscar -- Marigorta, Urko M -- Fernandez-Callejo, Marcos -- Prada, Maria Encina -- Encinas, Julio Manuel Vidal -- Nielsen, Rasmus -- Netea, Mihai G -- Novembre, John -- Sturm, Richard A -- Sabeti, Pardis -- Marques-Bonet, Tomas -- Navarro, Arcadi -- Willerslev, Eske -- Lalueza-Fox, Carles -- F32 GM106656/GM/NIGMS NIH HHS/ -- F32GM106656/GM/NIGMS NIH HHS/ -- R01 HG007089/HG/NHGRI NIH HHS/ -- R01-HG007089/HG/NHGRI NIH HHS/ -- England -- Nature. 2014 Mar 13;507(7491):225-8. doi: 10.1038/nature12960. Epub 2014 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Institut de Biologia Evolutiva, CSIC-UPF, Barcelona 08003, Spain [2]. ; 1] Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, DK-1350 Copenhagen K, Denmark [2]. ; Institut de Biologia Evolutiva, CSIC-UPF, Barcelona 08003, Spain. ; Department of Ecology and Evolutionary Biology, University of California, Los Angeles, California 90095, USA. ; 1] Department of Integrative Biology, University of California, Berkeley, California 94720, USA [2] Department of Biology, Pennsylvania State University, 502 Wartik Laboratory, University Park, Pennsylvania 16802, USA. ; Center for Biological Sequence Analysis, Technical University of Denmark, DK-2800 Kongens Lyngby, Denmark. ; I.E.S.O. 'Los Salados', Junta de Castilla y Leon, E-49600 Benavente, Spain. ; Junta de Castilla y Leon, Servicio de Cultura de Leon, E-24071 Leon, Spain. ; Center for Theoretical Evolutionary Genomics, University of California, Berkeley, California 94720, USA. ; Department of Medicine and Nijmegen Institute for Infection, Inflammation and Immunity, Radboud University Nijmegen Medical Centre, 6500 Nijmegen, The Netherlands. ; Department of Human Genetics, University of Chicago, Illinois 60637, USA. ; Institute for Molecular Bioscience, Melanogenix Group, The University of Queensland, Brisbane, Queensland 4072, Australia. ; 1] Center for Systems Biology, Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, Massachusetts 02138, USA [2] Broad Institute of the Massachusetts Institute of Technology and Harvard, Cambridge, Massachusetts 02142, USA. ; 1] Institut de Biologia Evolutiva, CSIC-UPF, Barcelona 08003, Spain [2] Institucio Catalana de Recerca i Estudis Avancats (ICREA), 08010 Barcelona, Catalonia, Spain. ; 1] Institut de Biologia Evolutiva, CSIC-UPF, Barcelona 08003, Spain [2] Institucio Catalana de Recerca i Estudis Avancats (ICREA), 08010 Barcelona, Catalonia, Spain [3] Centre de Regulacio Genomica (CRG), Barcelona 08003, Catalonia, Spain [4] National Institute for Bioinformatics (INB), Barcelona 08003, Catalonia, Spain. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, DK-1350 Copenhagen K, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24463515" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture/history ; *Alleles ; Biological Evolution ; Caves ; European Continental Ancestry Group/*genetics ; Eye Color/genetics ; *Fossils ; Genome, Human/genetics ; Genomics ; History, Ancient ; Humans ; Immunity/*genetics ; Lactose Intolerance/genetics ; Male ; Pigmentation/*genetics ; Polymorphism, Single Nucleotide/genetics ; Principal Component Analysis ; Skeleton ; Skin Pigmentation/genetics ; Spain/ethnology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2014-09-27
    Description: Monocyte differentiation into macrophages represents a cornerstone process for host defense. Concomitantly, immunological imprinting of either tolerance or trained immunity determines the functional fate of macrophages and susceptibility to secondary infections. We characterized the transcriptomes and epigenomes in four primary cell types: monocytes and in vitro-differentiated naive, tolerized, and trained macrophages. Inflammatory and metabolic pathways were modulated in macrophages, including decreased inflammasome activation, and we identified pathways functionally implicated in trained immunity. beta-glucan training elicits an exclusive epigenetic signature, revealing a complex network of enhancers and promoters. Analysis of transcription factor motifs in deoxyribonuclease I hypersensitive sites at cell-type-specific epigenetic loci unveiled differentiation and treatment-specific repertoires. Altogether, we provide a resource to understand the epigenetic changes that underlie innate immunity in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242194/" 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/PMC4242194/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saeed, Sadia -- Quintin, Jessica -- Kerstens, Hindrik H D -- Rao, Nagesha A -- Aghajanirefah, Ali -- Matarese, Filomena -- Cheng, Shih-Chin -- Ratter, Jacqueline -- Berentsen, Kim -- van der Ent, Martijn A -- Sharifi, Nilofar -- Janssen-Megens, Eva M -- Ter Huurne, Menno -- Mandoli, Amit -- van Schaik, Tom -- Ng, Aylwin -- Burden, Frances -- Downes, Kate -- Frontini, Mattia -- Kumar, Vinod -- Giamarellos-Bourboulis, Evangelos J -- Ouwehand, Willem H -- van der Meer, Jos W M -- Joosten, Leo A B -- Wijmenga, Cisca -- Martens, Joost H A -- Xavier, Ramnik J -- Logie, Colin -- Netea, Mihai G -- Stunnenberg, Hendrik G -- P30 DK043351/DK/NIDDK NIH HHS/ -- RG/09/012/28096/British Heart Foundation/United Kingdom -- New York, N.Y. -- Science. 2014 Sep 26;345(6204):1251086. doi: 10.1126/science.1251086.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Faculties of Science and Medicine, Radboud Institute for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. ; Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. ; Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard School of Medicine, Boston, MA 02114, USA. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA. ; Department of Haematology, University of Cambridge, Cambridge, UK. National Health Service, Blood and Transplant Cambridge Centre, Cambridge Biomedical Campus, Cambridge CB0 2PT, UK. ; University of Groningen, University Medical Center Groningen, Department of Genetics, Groningen, Netherlands. ; Fourth Department of Internal Medicine, University of Athens, Medical School, 1 Rimini Street, 12462 Athens, Greece. ; Department of Molecular Biology, Faculties of Science and Medicine, Radboud Institute for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. h.stunnenberg@ncmls.ru.nl mihai.netea@radboudumc.nl c.logie@ncmls.ru.nl. ; Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. h.stunnenberg@ncmls.ru.nl mihai.netea@radboudumc.nl c.logie@ncmls.ru.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25258085" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites/genetics ; Cell Differentiation/*genetics ; Deoxyribonuclease I/chemistry ; *Epigenesis, Genetic ; Genomic Imprinting ; Humans ; Immunity, Innate/*genetics ; Immunologic Memory ; Inflammasomes/genetics/immunology ; Macrophages/*cytology/immunology ; Mice ; Monocytes/*cytology/immunology ; Transcription Factors/metabolism ; beta-Glucans/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2010-05-15
    Description: Lombardi et al. (Reports, 23 October 2009, p. 585) reported detection of the human gammaretrovirus XMRV in the blood cells of patients with chronic fatigue syndrome (CFS). However, the patient description provided was incomplete. The inclusion of patients from a "CFS outbreak" previously linked with a viral infection, without confirmation in sporadic CFS cases, casts doubt on the role of XMRV in the pathogenesis of CFS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van der Meer, Jos W M -- Netea, Mihai G -- Galama, Jochem M D -- van Kuppeveld, Frank J M -- New York, N.Y. -- Science. 2010 May 14;328(5980):825; author reply 825. doi: 10.1126/science.1183906.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, Netherlands. j.vandermeer@aig.umcn.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466904" target="_blank"〉PubMed〈/a〉
    Keywords: Blood Cells/*virology ; Cohort Studies ; Cytokines/analysis ; Disease Outbreaks ; Epidemiologic Research Design ; Fatigue Syndrome, Chronic/epidemiology/immunology/*virology ; Gammaretrovirus/*isolation & purification ; Humans ; Retroviridae Infections/epidemiology/immunology/*virology ; Tumor Virus Infections/epidemiology/immunology/*virology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2014-09-27
    Description: Epigenetic reprogramming of myeloid cells, also known as trained immunity, confers nonspecific protection from secondary infections. Using histone modification profiles of human monocytes trained with the Candida albicans cell wall constituent beta-glucan, together with a genome-wide transcriptome, we identified the induced expression of genes involved in glucose metabolism. Trained monocytes display high glucose consumption, high lactate production, and a high ratio of nicotinamide adenine dinucleotide (NAD(+)) to its reduced form (NADH), reflecting a shift in metabolism with an increase in glycolysis dependent on the activation of mammalian target of rapamycin (mTOR) through a dectin-1-Akt-HIF-1alpha (hypoxia-inducible factor-1alpha) pathway. Inhibition of Akt, mTOR, or HIF-1alpha blocked monocyte induction of trained immunity, whereas the adenosine monophosphate-activated protein kinase activator metformin inhibited the innate immune response to fungal infection. Mice with a myeloid cell-specific defect in HIF-1alpha were unable to mount trained immunity against bacterial sepsis. Our results indicate that induction of aerobic glycolysis through an Akt-mTOR-HIF-1alpha pathway represents the metabolic basis of trained immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4226238/" 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/PMC4226238/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, Shih-Chin -- Quintin, Jessica -- Cramer, Robert A -- Shepardson, Kelly M -- Saeed, Sadia -- Kumar, Vinod -- Giamarellos-Bourboulis, Evangelos J -- Martens, Joost H A -- Rao, Nagesha Appukudige -- Aghajanirefah, Ali -- Manjeri, Ganesh R -- Li, Yang -- Ifrim, Daniela C -- Arts, Rob J W -- van der Veer, Brian M J W -- Deen, Peter M T -- Logie, Colin -- O'Neill, Luke A -- Willems, Peter -- van de Veerdonk, Frank L -- van der Meer, Jos W M -- Ng, Aylwin -- Joosten, Leo A B -- Wijmenga, Cisca -- Stunnenberg, Hendrik G -- Xavier, Ramnik J -- Netea, Mihai G -- 1P30GM106394-01/GM/NIGMS NIH HHS/ -- 5P30GM103415-03/GM/NIGMS NIH HHS/ -- DK097485/DK/NIDDK NIH HHS/ -- DK43351/DK/NIDDK NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- P30 GM103415/GM/NIGMS NIH HHS/ -- P30 GM106394/GM/NIGMS NIH HHS/ -- R01 AI081838/AI/NIAID NIH HHS/ -- R01 DK097485/DK/NIDDK NIH HHS/ -- R01AI81838/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 26;345(6204):1250684. doi: 10.1126/science.1250684.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. ; Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA. ; Department of Molecular Biology, Faculties of Science and Medicine, Nijmegen Centre for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. ; Department of Genetics, University of Groningen, University Medical Center Groningen, Groningen, Netherlands. ; 4th Department of Internal Medicine, University of Athens Medical School, 12462 Athens, Greece. ; Department of Biochemistry, Faculties of Science and Medicine, Nijmegen Centre for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. ; Department of Physiology, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. ; School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland. ; Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard School of Medicine, Boston, MA 02114, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. mihai.netea@radboudumc.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25258083" target="_blank"〉PubMed〈/a〉
    Keywords: Aerobiosis/immunology ; Animals ; Candida albicans/immunology ; Candidiasis/immunology/metabolism ; Disease Models, Animal ; *Epigenesis, Genetic ; Female ; Glucose/metabolism ; Glycolysis/*immunology ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics/*metabolism ; Immunity, Innate/*genetics ; Immunologic Memory/*genetics ; Male ; Mice ; Mice, Inbred C57BL ; Monocytes/*immunology/metabolism ; Sepsis/genetics/immunology/metabolism ; Staphylococcal Infections/immunology/metabolism ; Staphylococcus aureus ; TOR Serine-Threonine Kinases/genetics/*metabolism ; Transcriptome ; beta-Glucans/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2016-04-23
    Description: The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained immunity" or "innate immune memory." Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Netea, Mihai G -- Joosten, Leo A B -- Latz, Eicke -- Mills, Kingston H G -- Natoli, Gioacchino -- Stunnenberg, Hendrik G -- O'Neill, Luke A J -- Xavier, Ramnik J -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):aaf1098. doi: 10.1126/science.aaf1098. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, Netherlands. mihai.netea@radboudumc.nl. ; Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, Netherlands. ; Institute of Innate Immunity, Bonn University, Bonn, Germany. Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA. German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany. ; School of Biochemistry and Immunology, Trinity College, Dublin, Ireland. ; Department of Experimental Oncology, European Institute of Oncology, Milan, Italy. ; Department of Molecular Biology, Faculties of Science and Medicine, Radboud Institute of Molecular Life Sciences, Radboud University, Nijmegen, Netherlands. ; The Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102489" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Methylation ; Epigenesis, Genetic ; Histones/metabolism ; Humans ; Immunity, Innate/genetics/*immunology ; Immunologic Memory/genetics/*immunology ; Infection/*immunology ; Inflammation/immunology ; Invertebrates/immunology ; Plants/immunology ; Transcription, Genetic ; Vaccination ; Vaccines/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2016-04-30
    Description: Deep sequencing of the gut microbiomes of 1135 participants from a Dutch population-based cohort shows relations between the microbiome and 126 exogenous and intrinsic host factors, including 31 intrinsic factors, 12 diseases, 19 drug groups, 4 smoking categories, and 60 dietary factors. These factors collectively explain 18.7% of the variation seen in the interindividual distance of microbial composition. We could associate 110 factors to 125 species and observed that fecal chromogranin A (CgA), a protein secreted by enteroendocrine cells, was exclusively associated with 61 microbial species whose abundance collectively accounted for 53% of microbial composition. Low CgA concentrations were seen in individuals with a more diverse microbiome. These results are an important step toward a better understanding of environment-diet-microbe-host interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhernakova, Alexandra -- Kurilshikov, Alexander -- Bonder, Marc Jan -- Tigchelaar, Ettje F -- Schirmer, Melanie -- Vatanen, Tommi -- Mujagic, Zlatan -- Vila, Arnau Vich -- Falony, Gwen -- Vieira-Silva, Sara -- Wang, Jun -- Imhann, Floris -- Brandsma, Eelke -- Jankipersadsing, Soesma A -- Joossens, Marie -- Cenit, Maria Carmen -- Deelen, Patrick -- Swertz, Morris A -- LifeLines cohort study -- Weersma, Rinse K -- Feskens, Edith J M -- Netea, Mihai G -- Gevers, Dirk -- Jonkers, Daisy -- Franke, Lude -- Aulchenko, Yurii S -- Huttenhower, Curtis -- Raes, Jeroen -- Hofker, Marten H -- Xavier, Ramnik J -- Wijmenga, Cisca -- Fu, Jingyuan -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):565-9. doi: 10.1126/science.aad3369. Epub 2016 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Groningen, University Medical Center Groningen, Department of Genetics, Groningen, Netherlands. Top Institute Food and Nutrition, Wageningen, Netherlands. a.zhernakova@umcg.nl c.wijmenga@umcg.nl j.fu@umcg.nl. ; Institute of Chemical Biology and Fundamental Medicine SB RAS, Novosibirsk, Russia. Novosibirsk State University, Novosibirsk, Russia. ; University of Groningen, University Medical Center Groningen, Department of Genetics, Groningen, Netherlands. ; University of Groningen, University Medical Center Groningen, Department of Genetics, Groningen, Netherlands. Top Institute Food and Nutrition, Wageningen, Netherlands. ; The Broad Institute of MIT and Harvard, Cambridge, MA, USA. Department of Biostatistics, Harvard T. H. Chan School of Public Health, Boston, MA, USA. ; The Broad Institute of MIT and Harvard, Cambridge, MA, USA. Department of Computer Science, Aalto University School of Science, Espoo, Finland. ; Top Institute Food and Nutrition, Wageningen, Netherlands. Division of Gastroenterology-Hepatology, Department of Internal Medicine, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht, Netherlands. ; University of Groningen, University Medical Center Groningen, Department of Gastroenterology and Hepatology, Groningen, Netherlands. ; KU Leuven-University of Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Laboratory of Molecular Bacteriology, Leuven, Belgium. VIB, Center for the Biology of Disease, Leuven, Belgium. ; University of Groningen, University Medical Center Groningen, Department of Pediatrics, Groningen, Netherlands. ; KU Leuven-University of Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Laboratory of Molecular Bacteriology, Leuven, Belgium. VIB, Center for the Biology of Disease, Leuven, Belgium. Vrije Universiteit Brussel, Faculty of Sciences and Bioengineering Sciences, Microbiology Unit, Brussels, Belgium. ; University of Groningen, University Medical Center Groningen, Department of Genetics, Groningen, Netherlands. Microbial Ecology, Nutrition and Health Research Group, Institute of Agrochemistry and Food Technology, National Research Council (IATA-CSIC), Valencia, Spain. Department of Pediatrics, Dr. Peset University Hospital, Valencia, Spain. ; University of Groningen, University Medical Center Groningen, Department of Genetics, Groningen, Netherlands. University of Groningen, University Medical Center Groningen, Genomics Coordination Center, Groningen, Netherlands. ; Top Institute Food and Nutrition, Wageningen, Netherlands. Division of Human Nutrition, Wageningen University, Wageningen, Netherlands. ; Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, Netherlands. ; The Broad Institute of MIT and Harvard, Cambridge, MA, USA. ; Division of Gastroenterology-Hepatology, Department of Internal Medicine, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht, Netherlands. ; Novosibirsk State University, Novosibirsk, Russia. Centre for Global Health Research, Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Teviot Place, Edinburgh EH8 9AG, UK. PolyOmica, Groningen, Netherlands. Institute of Cytology and Genetics SB RAS, Novosibirsk, Russia. ; The Broad Institute of MIT and Harvard, Cambridge, MA, USA. Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, MA, USA. Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Boston, MA, USA. Center for Microbiome Informatics and Therapeutics, Massachusetts Institute of Technology, Cambridge, MA, USA. ; University of Groningen, University Medical Center Groningen, Department of Genetics, Groningen, Netherlands. a.zhernakova@umcg.nl c.wijmenga@umcg.nl j.fu@umcg.nl. ; University of Groningen, University Medical Center Groningen, Department of Genetics, Groningen, Netherlands. University of Groningen, University Medical Center Groningen, Department of Pediatrics, Groningen, Netherlands. a.zhernakova@umcg.nl c.wijmenga@umcg.nl j.fu@umcg.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126040" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteria/*classification/genetics/isolation & purification ; Chromogranin A/analysis/metabolism ; Diet ; Enteroendocrine Cells/metabolism ; Feces/chemistry/microbiology ; Gastrointestinal Microbiome/*genetics ; Gastrointestinal Tract/*microbiology ; Genetic Markers ; High-Throughput Nucleotide Sequencing ; Humans ; Metagenomics ; Netherlands ; Phylogeny ; RNA, Ribosomal, 16S/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2014-03-05
    Description: Patients with chronic granulomatous disease (CGD) have a mutated NADPH complex resulting in defective production of reactive oxygen species; these patients can develop severe colitis and are highly susceptible to invasive fungal infection. In NADPH oxidase-deficient mice, autophagy is defective but inflammasome activation is present despite lack of reactive oxygen...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 8
    Publication Date: 2011-03-07
    Print ISSN: 0027-8424
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  • 9
    Publication Date: 2008-02-22
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    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 10
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