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  • 1
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    Coinfection. Virus-helminth coinfection reveals a microbiota-independent mechanism of immunomodulation (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2014-08-02
    Beschreibung: The mammalian intestine is colonized by beneficial commensal bacteria and is a site of infection by pathogens, including helminth parasites. Helminths induce potent immunomodulatory effects, but whether these effects are mediated by direct regulation of host immunity or indirectly through eliciting changes in the microbiota is unknown. We tested this in the context of virus-helminth coinfection. Helminth coinfection resulted in impaired antiviral immunity and was associated with changes in the microbiota and STAT6-dependent helminth-induced alternative activation of macrophages. Notably, helminth-induced impairment of antiviral immunity was evident in germ-free mice, but neutralization of Ym1, a chitinase-like molecule that is associated with alternatively activated macrophages, could partially restore antiviral immunity. These data indicate that helminth-induced immunomodulation occurs independently of changes in the microbiota but is dependent on Ym1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548887/" 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/PMC4548887/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osborne, Lisa C -- Monticelli, Laurel A -- Nice, Timothy J -- Sutherland, Tara E -- Siracusa, Mark C -- Hepworth, Matthew R -- Tomov, Vesselin T -- Kobuley, Dmytro -- Tran, Sara V -- Bittinger, Kyle -- Bailey, Aubrey G -- Laughlin, Alice L -- Boucher, Jean-Luc -- Wherry, E John -- Bushman, Frederic D -- Allen, Judith E -- Virgin, Herbert W -- Artis, David -- 095831/Wellcome Trust/United Kingdom -- 2-P30 CA016520/CA/NCI NIH HHS/ -- 5T32A100716334/PHS HHS/ -- AI061570/AI/NIAID NIH HHS/ -- AI074878/AI/NIAID NIH HHS/ -- AI082630/AI/NIAID NIH HHS/ -- AI083022/AI/NIAID NIH HHS/ -- AI087990/AI/NIAID NIH HHS/ -- AI095466/AI/NIAID NIH HHS/ -- AI095608/AI/NIAID NIH HHS/ -- AI097333/AI/NIAID NIH HHS/ -- AI102942/AI/NIAID NIH HHS/ -- AI106697/AI/NIAID NIH HHS/ -- F32 AI085828/AI/NIAID NIH HHS/ -- F32-AI085828/AI/NIAID NIH HHS/ -- HHSN272201300006C/PHS HHS/ -- K08 DK097301/DK/NIDDK NIH HHS/ -- K08-DK097301/DK/NIDDK NIH HHS/ -- MR/J001929/1/Medical Research Council/United Kingdom -- P01 AI106697/AI/NIAID NIH HHS/ -- P30-AI045008/AI/NIAID NIH HHS/ -- P30-DK050306/DK/NIDDK NIH HHS/ -- R01 AI 084887/AI/NIAID NIH HHS/ -- R01 AI061570/AI/NIAID NIH HHS/ -- R01 AI074878/AI/NIAID NIH HHS/ -- R01 AI095466/AI/NIAID NIH HHS/ -- R01 AI097333/AI/NIAID NIH HHS/ -- R01 AI102942/AI/NIAID NIH HHS/ -- R21 AI087990/AI/NIAID NIH HHS/ -- T32-AI007532/AI/NIAID NIH HHS/ -- U01 AI095608/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 1;345(6196):578-82. doi: 10.1126/science.1256942. Epub 2014 Jul 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT, UK. ; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Medicine, Division of Gastroenterology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Medicine, Division of Gastroenterology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques, Universite Paris Descartes, Paris, France. ; Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. dartis@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25082704" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; CD8-Positive T-Lymphocytes/immunology ; Caliciviridae Infections/*immunology ; Coinfection/*immunology/microbiology/parasitology ; Gastroenteritis/*immunology/virology ; Germ-Free Life ; *Immunomodulation ; Intestines/immunology/microbiology/virology ; Lectins/*immunology ; Macrophage Activation ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Microbiota/*immunology ; Norovirus/*immunology ; Trichinella/*immunology ; Trichinellosis/*immunology ; beta-N-Acetylhexosaminidases/*immunology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Viral immunity. Transkingdom control of viral infection and immunity in the mammalian intestine (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2016-01-28
    Beschreibung: Viruses that infect the intestine include major human pathogens (retroviruses, noroviruses, rotaviruses, astroviruses, picornaviruses, adenoviruses, herpesviruses) that constitute a serious public health problem worldwide. These viral pathogens are members of a large, complex viral community inhabiting the intestine termed "the enteric virome." Enteric viruses have intimate functional and genetic relationships with both the host and other microbial constituents that inhabit the intestine, such as the bacterial microbiota, their associated phages, helminthes, and fungi, which together constitute the microbiome. Emerging data indicate that enteric viruses regulate, and are in turn regulated by, these other microbes through a series of processes termed "transkingdom interactions." This represents a changing paradigm in intestinal immunity to viral infection. Here we review recent advances in the field and propose new ways in which to conceptualize this important area.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4751997/" 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/PMC4751997/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfeiffer, Julie K -- Virgin, Herbert W -- R01 AI074668/AI/NIAID NIH HHS/ -- R01 AI111918/AI/NIAID NIH HHS/ -- R01 DK 101354/DK/NIDDK NIH HHS/ -- R21 AI114927/AI/NIAID NIH HHS/ -- R24 OD019793/OD/NIH HHS/ -- U19 AI109725/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270). pii: aad5872. doi: 10.1126/science.aad5872. Epub 2016 Jan 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. julie.pfeiffer@utsouthwestern.edu virgin@wustl.edu. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. julie.pfeiffer@utsouthwestern.edu virgin@wustl.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816384" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Bacteria/immunology/virology ; Bacteriophages/physiology ; Fungi/immunology ; Host-Pathogen Interactions/immunology ; Humans ; Intestinal Diseases/*immunology/*virology ; Intestines/*immunology/*virology ; Microbiota/*immunology ; Virus Diseases/*immunology ; Viruses/*immunology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Noncanonical autophagy inhibits the autoinflammatory, lupus-like response to dying cells (2016)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2016-04-21
    Beschreibung: Defects in clearance of dying cells have been proposed to underlie the pathogenesis of systemic lupus erythematosus (SLE). Mice lacking molecules associated with dying cell clearance develop SLE-like disease, and phagocytes from patients with SLE often display defective clearance and increased inflammatory cytokine production when exposed to dying cells in vitro. Previously, we and others described a form of noncanonical autophagy known as LC3-associated phagocytosis (LAP), in which phagosomes containing engulfed particles, including dying cells, recruit elements of the autophagy pathway to facilitate maturation of phagosomes and digestion of their contents. Genome-wide association studies have identified polymorphisms in the Atg5 (ref. 8) and possibly Atg7 (ref. 9) genes, involved in both canonical autophagy and LAP, as markers of a predisposition for SLE. Here we describe the consequences of defective LAP in vivo. Mice lacking any of several components of the LAP pathway show increased serum levels of inflammatory cytokines and autoantibodies, glomerular immune complex deposition, and evidence of kidney damage. When dying cells are injected into LAP-deficient mice, they are engulfed but not efficiently degraded and trigger acute elevation of pro-inflammatory cytokines but not anti-inflammatory interleukin (IL)-10. Repeated injection of dying cells into LAP-deficient, but not LAP-sufficient, mice accelerated the development of SLE-like disease, including increased serum levels of autoantibodies. By contrast, mice deficient in genes required for canonical autophagy but not LAP do not display defective dying cell clearance, inflammatory cytokine production, or SLE-like disease, and, like wild-type mice, produce IL-10 in response to dying cells. Therefore, defects in LAP, rather than canonical autophagy, can cause SLE-like phenomena, and may contribute to the pathogenesis of SLE.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860026/" 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/PMC4860026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez, Jennifer -- Cunha, Larissa D -- Park, Sunmin -- Yang, Mao -- Lu, Qun -- Orchard, Robert -- Li, Quan-Zhen -- Yan, Mei -- Janke, Laura -- Guy, Cliff -- Linkermann, Andreas -- Virgin, Herbert W -- Green, Douglas R -- 1ZIAES10328601/PHS HHS/ -- R01 AI040646/AI/NIAID NIH HHS/ -- R01 AI40646/AI/NIAID NIH HHS/ -- U19 AI109725/AI/NIAID NIH HHS/ -- ZIA ES103286-01/Intramural NIH HHS/ -- England -- Nature. 2016 May 5;533(7601):115-9. doi: 10.1038/nature17950. Epub 2016 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Immunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, North Carolina 27709, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Division of Nephrology and Hypertension, Christian-Albrechts-University, Kiel 24105, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27096368" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigen-Antibody Complex/metabolism ; Autoantibodies/blood ; *Autophagy/genetics ; Cytokines/biosynthesis/blood ; Inflammation/blood/genetics/*pathology ; Interleukin-10/biosynthesis ; Kidney/metabolism/pathology ; Lupus Erythematosus, Systemic/blood/genetics/*immunology/*pathology ; Male ; Mice ; Microtubule-Associated Proteins/metabolism ; Phagocytes/cytology/physiology ; Phagosomes/physiology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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