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  • 1
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    Innate immunity and intestinal microbiota in the development of Type 1 diabetes (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-09-23
    Description: Type 1 diabetes (T1D) is a debilitating autoimmune disease that results from T-cell-mediated destruction of insulin-producing beta-cells. Its incidence has increased during the past several decades in developed countries, suggesting that changes in the environment (including the human microbial environment) may influence disease pathogenesis. The incidence of spontaneous T1D in non-obese diabetic (NOD) mice can be affected by the microbial environment in the animal housing facility or by exposure to microbial stimuli, such as injection with mycobacteria or various microbial products. Here we show that specific pathogen-free NOD mice lacking MyD88 protein (an adaptor for multiple innate immune receptors that recognize microbial stimuli) do not develop T1D. The effect is dependent on commensal microbes because germ-free MyD88-negative NOD mice develop robust diabetes, whereas colonization of these germ-free MyD88-negative NOD mice with a defined microbial consortium (representing bacterial phyla normally present in human gut) attenuates T1D. We also find that MyD88 deficiency changes the composition of the distal gut microbiota, and that exposure to the microbiota of specific pathogen-free MyD88-negative NOD donors attenuates T1D in germ-free NOD recipients. Together, these findings indicate that interaction of the intestinal microbes with the innate immune system is a critical epigenetic factor modifying T1D predisposition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2574766/" 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/PMC2574766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wen, Li -- Ley, Ruth E -- Volchkov, Pavel Yu -- Stranges, Peter B -- Avanesyan, Lia -- Stonebraker, Austin C -- Hu, Changyun -- Wong, F Susan -- Szot, Gregory L -- Bluestone, Jeffrey A -- Gordon, Jeffrey I -- Chervonsky, Alexander V -- DK063452/DK/NIDDK NIH HHS/ -- DK30292/DK/NIDDK NIH HHS/ -- DK42086/DK/NIDDK NIH HHS/ -- DK45735/DK/NIDDK NIH HHS/ -- DK70977/DK/NIDDK NIH HHS/ -- P30 DK042086/DK/NIDDK NIH HHS/ -- P30 DK042086-16/DK/NIDDK NIH HHS/ -- P30 DK045735/DK/NIDDK NIH HHS/ -- P30 DK045735-10/DK/NIDDK NIH HHS/ -- P30 DK045735-119006/DK/NIDDK NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30 DK056341-07/DK/NIDDK NIH HHS/ -- P30 DK056341-08/DK/NIDDK NIH HHS/ -- P30 DK063720/DK/NIDDK NIH HHS/ -- P30 DK063720-01/DK/NIDDK NIH HHS/ -- P30 DK63720/DK/NIDDK NIH HHS/ -- R01 DK030292/DK/NIDDK NIH HHS/ -- R01 DK030292-24/DK/NIDDK NIH HHS/ -- R01 DK070977/DK/NIDDK NIH HHS/ -- R01 DK070977-04/DK/NIDDK NIH HHS/ -- R21 DK063452/DK/NIDDK NIH HHS/ -- R21 DK063452-02/DK/NIDDK NIH HHS/ -- R37 AI046643/AI/NIAID NIH HHS/ -- R37 AI046643-10/AI/NIAID NIH HHS/ -- R37 AI46643/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Oct 23;455(7216):1109-13. doi: 10.1038/nature07336. Epub 2008 Sep 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18806780" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/classification/genetics/*immunology/isolation & purification ; CD8-Positive T-Lymphocytes/immunology ; Diabetes Mellitus, Type 1/genetics/*immunology/*microbiology ; Female ; Immunity, Innate/genetics/*immunology ; Interferon-gamma/immunology ; Intestines/*microbiology ; Islets of Langerhans/pathology ; Male ; Mice ; Mice, Inbred NOD ; Mice, Knockout ; Mice, SCID ; Molecular Sequence Data ; Myeloid Differentiation Factor 88/genetics ; Phylogeny ; Specific Pathogen-Free Organisms ; Time Factors
    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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    A core gut microbiome in obese and lean twins (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-12-02
    Description: The human distal gut harbours a vast ensemble of microbes (the microbiota) that provide important metabolic capabilities, including the ability to extract energy from otherwise indigestible dietary polysaccharides. Studies of a few unrelated, healthy adults have revealed substantial diversity in their gut communities, as measured by sequencing 16S rRNA genes, yet how this diversity relates to function and to the rest of the genes in the collective genomes of the microbiota (the gut microbiome) remains obscure. Studies of lean and obese mice suggest that the gut microbiota affects energy balance by influencing the efficiency of calorie harvest from the diet, and how this harvested energy is used and stored. Here we characterize the faecal microbial communities of adult female monozygotic and dizygotic twin pairs concordant for leanness or obesity, and their mothers, to address how host genotype, environmental exposure and host adiposity influence the gut microbiome. Analysis of 154 individuals yielded 9,920 near full-length and 1,937,461 partial bacterial 16S rRNA sequences, plus 2.14 gigabases from their microbiomes. The results reveal that the human gut microbiome is shared among family members, but that each person's gut microbial community varies in the specific bacterial lineages present, with a comparable degree of co-variation between adult monozygotic and dizygotic twin pairs. However, there was a wide array of shared microbial genes among sampled individuals, comprising an extensive, identifiable 'core microbiome' at the gene, rather than at the organismal lineage, level. Obesity is associated with phylum-level changes in the microbiota, reduced bacterial diversity and altered representation of bacterial genes and metabolic pathways. These results demonstrate that a diversity of organismal assemblages can nonetheless yield a core microbiome at a functional level, and that deviations from this core are associated with different physiological states (obese compared with lean).〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2677729/" 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/PMC2677729/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turnbaugh, Peter J -- Hamady, Micah -- Yatsunenko, Tanya -- Cantarel, Brandi L -- Duncan, Alexis -- Ley, Ruth E -- Sogin, Mitchell L -- Jones, William J -- Roe, Bruce A -- Affourtit, Jason P -- Egholm, Michael -- Henrissat, Bernard -- Heath, Andrew C -- Knight, Rob -- Gordon, Jeffrey I -- AA09022/AA/NIAAA NIH HHS/ -- DK78669/DK/NIDDK NIH HHS/ -- ES012742/ES/NIEHS NIH HHS/ -- HD049024/HD/NICHD NIH HHS/ -- P01 DK078669/DK/NIDDK NIH HHS/ -- P01 DK078669-01/DK/NIDDK NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30 DK056341-07/DK/NIDDK NIH HHS/ -- P30 DK056341-08/DK/NIDDK NIH HHS/ -- P50 ES012742/ES/NIEHS NIH HHS/ -- P50 ES012742-049001/ES/NIEHS NIH HHS/ -- R01 AA009022/AA/NIAAA NIH HHS/ -- R01 AA009022-10/AA/NIAAA NIH HHS/ -- R01 HD049024/HD/NICHD NIH HHS/ -- R01 HD049024-01/HD/NICHD NIH HHS/ -- T32 GM065103/GM/NIGMS NIH HHS/ -- T32 GM065103-07/GM/NIGMS NIH HHS/ -- UL1 TR000448/TR/NCATS NIH HHS/ -- England -- Nature. 2009 Jan 22;457(7228):480-4. doi: 10.1038/nature07540. Epub 2008 Nov 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences, Washington University School of Medicine, St Louis, Missouri 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19043404" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Africa/ethnology ; Biodiversity ; Environment ; Europe/ethnology ; Feces/microbiology ; Female ; Gastrointestinal Tract/*microbiology ; Genotype ; Humans ; Metagenome/genetics/*physiology ; Missouri ; Molecular Sequence Data ; Mothers ; Obesity/*microbiology ; RNA, Ribosomal, 16S/analysis/genetics ; Thinness/*microbiology ; Twins, Dizygotic ; Twins, Monozygotic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Evolution of mammals and their gut microbes (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-24
    Description: Mammals are metagenomic in that they are composed of not only their own gene complements but also those of all of their associated microbes. To understand the coevolution of the mammals and their indigenous microbial communities, we conducted a network-based analysis of bacterial 16S ribosomal RNA gene sequences from the fecal microbiota of humans and 59 other mammalian species living in two zoos and in the wild. The results indicate that host diet and phylogeny both influence bacterial diversity, which increases from carnivory to omnivory to herbivory; that bacterial communities codiversified with their hosts; and that the gut microbiota of humans living a modern life-style is typical of omnivorous primates.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2649005/" 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/PMC2649005/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ley, Ruth E -- Hamady, Micah -- Lozupone, Catherine -- Turnbaugh, Peter J -- Ramey, Rob Roy -- Bircher, J Stephen -- Schlegel, Michael L -- Tucker, Tammy A -- Schrenzel, Mark D -- Knight, Rob -- Gordon, Jeffrey I -- DK30292/DK/NIDDK NIH HHS/ -- DK70977/DK/NIDDK NIH HHS/ -- DK78669/DK/NIDDK NIH HHS/ -- P01 DK078669/DK/NIDDK NIH HHS/ -- P01 DK078669-02/DK/NIDDK NIH HHS/ -- R01 DK030292/DK/NIDDK NIH HHS/ -- R01 DK030292-24/DK/NIDDK NIH HHS/ -- R01 DK070977/DK/NIDDK NIH HHS/ -- R01 DK070977-04/DK/NIDDK NIH HHS/ -- T32 GM065103/GM/NIGMS NIH HHS/ -- T32 GM065103-07/GM/NIGMS NIH HHS/ -- T32GM065103/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 20;320(5883):1647-51. doi: 10.1126/science.1155725. Epub 2008 May 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences, Washington University School of Medicine, St. Louis, MO 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497261" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Animals, Wild/classification/genetics/microbiology ; Animals, Zoo/classification/genetics/microbiology ; Bacteria/*classification/genetics/isolation & purification ; *Bacterial Physiological Phenomena ; *Biological Evolution ; Carnivora/classification/genetics/microbiology ; *Diet ; Feces/microbiology ; Gastrointestinal Tract/*microbiology ; Genes, rRNA ; Humans ; Mammals/classification/genetics/*microbiology ; Molecular Sequence Data ; *Phylogeny ; Primates/classification/genetics/microbiology ; RNA, Ribosomal, 16S/genetics
    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
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    Metabolic syndrome and altered gut microbiota in mice lacking Toll-like receptor 5 (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-03-06
    Description: Metabolic syndrome is a group of obesity-related metabolic abnormalities that increase an individual's risk of developing type 2 diabetes and cardiovascular disease. Here, we show that mice genetically deficient in Toll-like receptor 5 (TLR5), a component of the innate immune system that is expressed in the gut mucosa and that helps defend against infection, exhibit hyperphagia and develop hallmark features of metabolic syndrome, including hyperlipidemia, hypertension, insulin resistance, and increased adiposity. These metabolic changes correlated with changes in the composition of the gut microbiota, and transfer of the gut microbiota from TLR5-deficient mice to wild-type germ-free mice conferred many features of metabolic syndrome to the recipients. Food restriction prevented obesity, but not insulin resistance, in the TLR5-deficient mice. These results support the emerging view that the gut microbiota contributes to metabolic disease and suggest that malfunction of the innate immune system may promote the development of metabolic syndrome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4714868/" 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/PMC4714868/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vijay-Kumar, Matam -- Aitken, Jesse D -- Carvalho, Frederic A -- Cullender, Tyler C -- Mwangi, Simon -- Srinivasan, Shanthi -- Sitaraman, Shanthi V -- Knight, Rob -- Ley, Ruth E -- Gewirtz, Andrew T -- DK061417/DK/NIDDK NIH HHS/ -- DK06439/DK/NIDDK NIH HHS/ -- DK083275/DK/NIDDK NIH HHS/ -- K01 DK083275/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Apr 9;328(5975):228-31. doi: 10.1126/science.1179721. Epub 2010 Mar 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Emory University, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203013" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bacterial Physiological Phenomena ; Blood Glucose/analysis ; Body Fat Distribution ; Body Weight ; Caloric Restriction ; Dietary Fats/administration & dosage ; Female ; Germ-Free Life ; Hyperphagia/etiology ; *Immunity, Innate ; Insulin Resistance ; Intestinal Mucosa/immunology ; Intestines/*microbiology ; Male ; Metabolic Syndrome X/*etiology/immunology/microbiology ; Mice ; Mice, Knockout ; Obesity/etiology/immunology/microbiology/prevention & control ; Toll-Like Receptor 5/deficiency/genetics/*metabolism
    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
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    Host-bacterial mutualism in the human intestine (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-03-26
    Description: The distal human intestine represents an anaerobic bioreactor programmed with an enormous population of bacteria, dominated by relatively few divisions that are highly diverse at the strain/subspecies level. This microbiota and its collective genomes (microbiome) provide us with genetic and metabolic attributes we have not been required to evolve on our own, including the ability to harvest otherwise inaccessible nutrients. New studies are revealing how the gut microbiota has coevolved with us and how it manipulates and complements our biology in ways that are mutually beneficial. We are also starting to understand how certain keystone members of the microbiota operate to maintain the stability and functional adaptability of this microbial organ.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Backhed, Fredrik -- Ley, Ruth E -- Sonnenburg, Justin L -- Peterson, Daniel A -- Gordon, Jeffrey I -- New York, N.Y. -- Science. 2005 Mar 25;307(5717):1915-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences, Washington University School of Medicine, St. Louis, MO 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15790844" target="_blank"〉PubMed〈/a〉
    Keywords: Anaerobiosis ; Bacteria/classification ; *Bacterial Physiological Phenomena ; Bacteroides/genetics/physiology ; Biodiversity ; Biological Evolution ; Ecosystem ; Energy Intake ; Energy Metabolism ; Gastrointestinal Tract/*microbiology/physiology ; Genome, Bacterial ; Humans ; Intestines/*microbiology/physiology ; Obesity/etiology ; Selection, Genetic
    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
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    Defining the core Arabidopsis thaliana root microbiome (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-08-04
    Description: Land plants associate with a root microbiota distinct from the complex microbial community present in surrounding soil. The microbiota colonizing the rhizosphere (immediately surrounding the root) and the endophytic compartment (within the root) contribute to plant growth, productivity, carbon sequestration and phytoremediation. Colonization of the root occurs despite a sophisticated plant immune system, suggesting finely tuned discrimination of mutualists and commensals from pathogens. Genetic principles governing the derivation of host-specific endophyte communities from soil communities are poorly understood. Here we report the pyrosequencing of the bacterial 16S ribosomal RNA gene of more than 600 Arabidopsis thaliana plants to test the hypotheses that the root rhizosphere and endophytic compartment microbiota of plants grown under controlled conditions in natural soils are sufficiently dependent on the host to remain consistent across different soil types and developmental stages, and sufficiently dependent on host genotype to vary between inbred Arabidopsis accessions. We describe different bacterial communities in two geochemically distinct bulk soils and in rhizosphere and endophytic compartments prepared from roots grown in these soils. The communities in each compartment are strongly influenced by soil type. Endophytic compartments from both soils feature overlapping, low-complexity communities that are markedly enriched in Actinobacteria and specific families from other phyla, notably Proteobacteria. Some bacteria vary quantitatively between plants of different developmental stage and genotype. Our rigorous definition of an endophytic compartment microbiome should facilitate controlled dissection of plant-microbe interactions derived from complex soil communities.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4074413/" 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/PMC4074413/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lundberg, Derek S -- Lebeis, Sarah L -- Paredes, Sur Herrera -- Yourstone, Scott -- Gehring, Jase -- Malfatti, Stephanie -- Tremblay, Julien -- Engelbrektson, Anna -- Kunin, Victor -- del Rio, Tijana Glavina -- Edgar, Robert C -- Eickhorst, Thilo -- Ley, Ruth E -- Hugenholtz, Philip -- Tringe, Susannah Green -- Dangl, Jeffery L -- K12GM000678/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Aug 2;488(7409):86-90. doi: 10.1038/nature11237.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of North Carolina, Chapel Hill, North Carolina 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22859206" target="_blank"〉PubMed〈/a〉
    Keywords: Actinobacteria/genetics/isolation & purification ; Arabidopsis/classification/growth & development/*microbiology ; Endophytes/*classification/genetics/*isolation & purification ; Genotype ; In Situ Hybridization, Fluorescence ; *Metagenome ; Plant Roots/classification/growth & development/*microbiology ; Proteobacteria/genetics/isolation & purification ; RNA, Ribosomal, 16S/genetics/isolation & purification ; Rhizosphere ; Ribotyping ; Sequence Analysis, DNA ; *Soil Microbiology ; Symbiosis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Nutrition: When guests turn hostile (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ley, Ruth E -- England -- Nature. 2013 Feb 28;494(7438):437-8. doi: 10.1038/494437a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23446414" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology/*therapeutic use ; Case-Control Studies ; Child, Preschool ; *Diet Therapy ; Feces/microbiology ; Germ-Free Life ; Health ; Humans ; Infant ; Infant, Newborn ; Kwashiorkor/diet therapy/epidemiology/etiology/microbiology ; Malawi/epidemiology ; Malnutrition/etiology/*microbiology/physiopathology/*therapy ; Mice ; Nutrition Processes/drug effects ; Probiotics/therapeutic use ; Risk Factors ; Survival Rate ; Symbiosis ; Twin Studies as Topic ; Weight Loss/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-03-04
    Description: The intestinal tract is inhabited by a large and diverse community of microbes collectively referred to as the gut microbiota. While the gut microbiota provides important benefits to its host, especially in metabolism and immune development, disturbance of the microbiota-host relationship is associated with numerous chronic inflammatory diseases, including inflammatory bowel disease and the group of obesity-associated diseases collectively referred to as metabolic syndrome. A primary means by which the intestine is protected from its microbiota is via multi-layered mucus structures that cover the intestinal surface, thereby allowing the vast majority of gut bacteria to be kept at a safe distance from epithelial cells that line the intestine. Thus, agents that disrupt mucus-bacterial interactions might have the potential to promote diseases associated with gut inflammation. Consequently, it has been hypothesized that emulsifiers, detergent-like molecules that are a ubiquitous component of processed foods and that can increase bacterial translocation across epithelia in vitro, might be promoting the increase in inflammatory bowel disease observed since the mid-twentieth century. Here we report that, in mice, relatively low concentrations of two commonly used emulsifiers, namely carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type hosts and promoted robust colitis in mice predisposed to this disorder. Emulsifier-induced metabolic syndrome was associated with microbiota encroachment, altered species composition and increased pro-inflammatory potential. Use of germ-free mice and faecal transplants indicated that such changes in microbiota were necessary and sufficient for both low-grade inflammation and metabolic syndrome. These results support the emerging concept that perturbed host-microbiota interactions resulting in low-grade inflammation can promote adiposity and its associated metabolic effects. Moreover, they suggest that the broad use of emulsifying agents might be contributing to an increased societal incidence of obesity/metabolic syndrome and other chronic inflammatory diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chassaing, Benoit -- Koren, Omry -- Goodrich, Julia K -- Poole, Angela C -- Srinivasan, Shanthi -- Ley, Ruth E -- Gewirtz, Andrew T -- DK083890/DK/NIDDK NIH HHS/ -- DK099071/DK/NIDDK NIH HHS/ -- R01 DK083890/DK/NIDDK NIH HHS/ -- R01 DK099071/DK/NIDDK NIH HHS/ -- England -- Nature. 2015 Mar 5;519(7541):92-6. doi: 10.1038/nature14232. Epub 2015 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia 30303, USA. ; Faculty of Medicine, Bar Ilan University, Safed, 13115, Israel. ; Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853, USA. ; Digestive Diseases Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25731162" target="_blank"〉PubMed〈/a〉
    Keywords: Adiposity/drug effects ; Animals ; Carboxymethylcellulose Sodium/administration & dosage/adverse effects ; Colitis/*chemically induced/*microbiology/pathology ; Diet/*adverse effects ; Emulsifying Agents/administration & dosage/*adverse effects ; Feces/microbiology ; Female ; Gastrointestinal Tract/*drug effects/*microbiology/pathology ; Germ-Free Life ; Inflammation/chemically induced/microbiology/pathology ; Intestinal Mucosa/drug effects/microbiology/pathology ; Male ; Metabolic Syndrome X/*chemically induced/*microbiology/pathology ; Mice ; Microbiota/drug effects ; Obesity/chemically induced/microbiology/pathology ; Polysorbates/administration & dosage/adverse effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    The gene-microbe link (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ley, Ruth E -- England -- Nature. 2015 Feb 26;518(7540):S7. doi: 10.1038/518S7a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cornell University.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25715280" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Genetic Predisposition to Disease ; Germ-Free Life ; Gram-Positive Bacteria/physiology ; Humans ; Inflammatory Bowel Diseases/genetics/microbiology ; Intestines/microbiology ; Mice ; Microbiota/immunology/*physiology ; Obesity/etiology/genetics/microbiology/therapy ; Sample Size ; Symbiosis ; Thinness/etiology/genetics/microbiology ; Twin Studies as Topic ; Twins/genetics
    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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  • 10
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    Cross-species comparisons of host genetic associations with the microbiome (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-04-30
    Description: Recent studies in human populations and mouse models reveal notable congruences in gut microbial taxa whose abundances are partly regulated by host genotype. Host genes associating with these taxa are related to diet sensing, metabolism, and immunity. These broad patterns are further validated in similar studies of nonmammalian microbiomes. The next generation of genome-wide association studies will expand the size of the data sets and refine the microbial phenotypes to fully capture these intriguing signatures of host-microbiome coevolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodrich, Julia K -- Davenport, Emily R -- Waters, Jillian L -- Clark, Andrew G -- Ley, Ruth E -- R01 DK093595/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):532-5. doi: 10.1126/science.aad9379.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. ; Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tubingen, Germany. ; Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. Department of Microbiology, Cornell University, Ithaca NY, USA. Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tubingen, Germany. rel222@cornell.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126034" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/*classification/genetics ; Diet ; *Genome-Wide Association Study ; Genotype ; Humans ; Mice ; Microbiota/genetics/*physiology ; Phenotype ; *Quantitative Trait Loci ; Species Specificity
    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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