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  • 1
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    Innate and adaptive immunity cooperate flexibly to maintain host-microbiota mutualism (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-01
    Description: Commensal bacteria in the lower intestine of mammals are 10 times as numerous as the body's cells. We investigated the relative importance of different immune mechanisms in limiting the spread of the intestinal microbiota. Here, we reveal a flexible continuum between innate and adaptive immune function in containing commensal microbes. Mice deficient in critical innate immune functions such as Toll-like receptor signaling or oxidative burst production spontaneously produce high-titer serum antibodies against their commensal microbiota. These antibody responses are functionally essential to maintain host-commensal mutualism in vivo in the face of innate immune deficiency. Spontaneous hyper-activation of adaptive immunity against the intestinal microbiota, secondary to innate immune deficiency, may clarify the underlying mechanisms of inflammatory diseases where immune dysfunction is implicated.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3730530/" 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/PMC3730530/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slack, Emma -- Hapfelmeier, Siegfried -- Stecher, Barbel -- Velykoredko, Yuliya -- Stoel, Maaike -- Lawson, Melissa A E -- Geuking, Markus B -- Beutler, Bruce -- Tedder, Thomas F -- Hardt, Wolf-Dietrich -- Bercik, Premysl -- Verdu, Elena F -- McCoy, Kathy D -- Macpherson, Andrew J -- AI56363/AI/NIAID NIH HHS/ -- CA105001/CA/NCI NIH HHS/ -- R01 CA105001/CA/NCI NIH HHS/ -- U19 AI056363/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 31;325(5940):617-20. doi: 10.1126/science.1172747.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON L8S 4L8, Canada. andrew.macpherson@insel.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19644121" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Bacterial/biosynthesis/blood/*immunology ; Bacteremia/immunology/microbiology ; Bacteria/growth & development/*immunology/isolation & purification ; Bacterial Infections/immunology/microbiology ; CD4-Positive T-Lymphocytes/immunology ; Colony Count, Microbial ; Enterococcus faecalis/growth & development/immunology/isolation & purification ; Escherichia coli K12/growth & development/immunology/isolation & purification ; Germ-Free Life ; Immunity ; *Immunity, Innate ; Intestinal Mucosa/immunology/*microbiology ; Intestines/immunology/*microbiology ; Lymphoid Tissue/microbiology ; Mice ; Mice, Inbred C57BL ; Permeability ; Respiratory Burst ; Signal Transduction ; Specific Pathogen-Free Organisms ; Spleen/microbiology ; Toll-Like Receptors/genetics/*metabolism
    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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  • 2
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    Acquisition of a multifunctional IgA+ plasma cell phenotype in the gut (2011)
    Nature Publishing Group (NPG)
    Details
    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
    Published by Nature Publishing Group (NPG)
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  • 3
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    Reversible microbial colonization of germ-free mice reveals the dynamics of IgA immune responses (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-26
    Description: The lower intestine of adult mammals is densely colonized with nonpathogenic (commensal) microbes. Gut bacteria induce protective immune responses, which ensure host-microbial mutualism. The continuous presence of commensal intestinal bacteria has made it difficult to study mucosal immune dynamics. Here, we report a reversible germ-free colonization system in mice that is independent of diet or antibiotic manipulation. A slow (more than 14 days) onset of a long-lived (half-life over 16 weeks), highly specific anticommensal immunoglobulin A (IgA) response in germ-free mice was observed. Ongoing commensal exposure in colonized mice rapidly abrogated this response. Sequential doses lacked a classical prime-boost effect seen in systemic vaccination, but specific IgA induction occurred as a stepwise response to current bacterial exposure, such that the antibody repertoire matched the existing commensal content.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3923373/" 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/PMC3923373/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hapfelmeier, Siegfried -- Lawson, Melissa A E -- Slack, Emma -- Kirundi, Jorum K -- Stoel, Maaike -- Heikenwalder, Mathias -- Cahenzli, Julia -- Velykoredko, Yuliya -- Balmer, Maria L -- Endt, Kathrin -- Geuking, Markus B -- Curtiss, Roy 3rd -- McCoy, Kathy D -- Macpherson, Andrew J -- R01 AI060557/AI/NIAID NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1705-9. doi: 10.1126/science.1188454.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DKF (Maurice Muller Laboratories), MEM, Universitatsklinik fur Viszerale Chirurgie und Medizin (UVCM), University of Bern, 3013 Bern, Switzerland. hapfelmeier@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20576892" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Bacterial/biosynthesis/*immunology ; Antibody Specificity ; Colony Count, Microbial ; Dose-Response Relationship, Immunologic ; Escherichia coli/*growth & development/*immunology ; Germ-Free Life ; Half-Life ; Immunoglobulin A/biosynthesis/*immunology ; Immunologic Memory ; Intestinal Mucosa/*immunology/*microbiology ; Intestines/immunology/microbiology ; Mice ; Mice, Inbred C57BL ; Mucous Membrane/immunology ; Plasma Cells/immunology ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Sex differences in the gut microbiome drive hormone-dependent regulation of autoimmunity (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-01-19
    Description: Microbial exposures and sex hormones exert potent effects on autoimmune diseases, many of which are more prevalent in women. We demonstrate that early-life microbial exposures determine sex hormone levels and modify progression to autoimmunity in the nonobese diabetic (NOD) mouse model of type 1 diabetes (T1D). Colonization by commensal microbes elevated serum testosterone and protected NOD males from T1D. Transfer of gut microbiota from adult males to immature females altered the recipient's microbiota, resulting in elevated testosterone and metabolomic changes, reduced islet inflammation and autoantibody production, and robust T1D protection. These effects were dependent on androgen receptor activity. Thus, the commensal microbial community alters sex hormone levels and regulates autoimmune disease fate in individuals with high genetic risk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Markle, Janet G M -- Frank, Daniel N -- Mortin-Toth, Steven -- Robertson, Charles E -- Feazel, Leah M -- Rolle-Kampczyk, Ulrike -- von Bergen, Martin -- McCoy, Kathy D -- Macpherson, Andrew J -- Danska, Jayne S -- 64216/Canadian Institutes of Health Research/Canada -- R21HG005964/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 1;339(6123):1084-8. doi: 10.1126/science.1233521. Epub 2013 Jan 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Genetics and Genome Biology, Hospital for Sick Children Research Institute, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23328391" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autoimmunity ; Cecum/microbiology ; Diabetes Mellitus, Type 1/*microbiology ; Female ; Gonadal Steroid Hormones/*immunology ; Intestines/*microbiology ; Male ; *Metagenome ; Mice ; Mice, Inbred NOD ; *Sex Characteristics
    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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    The maternal microbiota drives early postnatal innate immune development (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-03-19
    Description: Postnatal colonization of the body with microbes is assumed to be the main stimulus to postnatal immune development. By transiently colonizing pregnant female mice, we show that the maternal microbiota shapes the immune system of the offspring. Gestational colonization increases intestinal group 3 innate lymphoid cells and F4/80(+)CD11c(+) mononuclear cells in the pups. Maternal colonization reprograms intestinal transcriptional profiles of the offspring, including increased expression of genes encoding epithelial antibacterial peptides and metabolism of microbial molecules. Some of these effects are dependent on maternal antibodies that potentially retain microbial molecules and transmit them to the offspring during pregnancy and in milk. Pups born to mothers transiently colonized in pregnancy are better able to avoid inflammatory responses to microbial molecules and penetration of intestinal microbes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gomez de Aguero, Mercedes -- Ganal-Vonarburg, Stephanie C -- Fuhrer, Tobias -- Rupp, Sandra -- Uchimura, Yasuhiro -- Li, Hai -- Steinert, Anna -- Heikenwalder, Mathias -- Hapfelmeier, Siegfried -- Sauer, Uwe -- McCoy, Kathy D -- Macpherson, Andrew J -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1296-302. doi: 10.1126/science.aad2571.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Maurice Muller Laboratories (DKF), Universitatsklinik fur Viszerale Chirurgie und Medizin Inselspital, Murtenstrasse 35, University of Bern, 3010 Bern, Switzerland. ; Institute of Molecular Systems Biology, Swiss Federal Institute of Technology (ETH) Zurich, 8093 Zurich, Switzerland. ; Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany. ; Institute for Infectious Diseases, University of Bern, 3010 Bern, Switzerland. ; Maurice Muller Laboratories (DKF), Universitatsklinik fur Viszerale Chirurgie und Medizin Inselspital, Murtenstrasse 35, University of Bern, 3010 Bern, Switzerland. andrew.macpherson@insel.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989247" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Escherichia coli/immunology ; Female ; Gastrointestinal Microbiome/*immunology ; Germ-Free Life ; Immune System/*growth & development/*microbiology ; Immunity, Innate/genetics/*immunology ; Immunity, Maternally-Acquired/genetics/*immunology ; Intestines/*immunology ; Lymphocytes/immunology ; Mice ; Mice, Inbred C57BL ; Pregnancy ; Symbiosis ; Transcription, Genetic
    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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  • 6
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    Maternal microbiota in pregnancy and early life (2019)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2019
    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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  • 7
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    Spatial genetic structure of the ectoparasite Ixodes uriae within breeding cliffs of its colonial seabird host (2003)
    Springer Nature
    Details
    Publication Date: 2003-09-26
    Print ISSN: 0018-067X
    Electronic ISSN: 1365-2540
    Topics: Biology
    Published by Springer Nature
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  • 8
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    When things go wrong: intra-season dynamics of breeding failure in a seabird (2014)
    Wiley
    Details
    Publication Date: 2014-01-01
    Electronic ISSN: 2150-8925
    Topics: Energy, Environment Protection, Nuclear Power Engineering
    Published by Wiley on behalf of Ecological Society of America.
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  • 9
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    Trans-oceanic host dispersal explains high seabird tick diversity on Cape Verde islands (2012)
    The Royal Society
    Details
    Publication Date: 2012-04-18
    Description: Parasites represent ideal models for unravelling biogeographic patterns and mechanisms of diversification on islands. Both host-mediated dispersal and within-island adaptation can shape parasite island assemblages. In this study, we examined patterns of genetic diversity and structure of Ornithodoros seabird ticks within the Cape Verde Archipelago in relation to their global phylogeography. Contrary to expectations, ticks from multiple, geographically distant clades mixed within the archipelago. Trans-oceanic colonization via host movements probably explains high local tick diversity, contrasting with previous research that suggests little large-scale dispersal in these birds. Although host specificity was not obvious at a global scale, host-associated genetic structure was found within Cape Verde colonies, indicating that post-colonization adaptation to specific hosts probably occurs. These results highlight the role of host metapopulation dynamics in the evolutionary ecology and epidemiology of avian parasites and pathogens.
    Print ISSN: 1744-9561
    Electronic ISSN: 1744-957X
    Topics: Biology
    Published by The Royal Society
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