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  • Homeostasis  (2)
  • American Association for the Advancement of Science (AAAS)  (2)
  • 1
    Publikationsdatum: 2011-10-15
    Beschreibung: The mammalian intestine is home to ~100 trillion bacteria that perform important metabolic functions for their hosts. The proximity of vast numbers of bacteria to host intestinal tissues raises the question of how symbiotic host-bacterial relationships are maintained without eliciting potentially harmful immune responses. Here, we show that RegIIIgamma, a secreted antibacterial lectin, is essential for maintaining a ~50-micrometer zone that physically separates the microbiota from the small intestinal epithelial surface. Loss of host-bacterial segregation in RegIIIgamma(-/-) mice was coupled to increased bacterial colonization of the intestinal epithelial surface and enhanced activation of intestinal adaptive immune responses by the microbiota. Together, our findings reveal that RegIIIgamma is a fundamental immune mechanism that promotes host-bacterial mutualism by regulating the spatial relationships between microbiota and host.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321924/" 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/PMC3321924/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vaishnava, Shipra -- Yamamoto, Miwako -- Severson, Kari M -- Ruhn, Kelly A -- Yu, Xiaofei -- Koren, Omry -- Ley, Ruth -- Wakeland, Edward K -- Hooper, Lora V -- R01 DK070855/DK/NIDDK NIH HHS/ -- R01 DK070855-06/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Oct 14;334(6053):255-8. doi: 10.1126/science.1209791.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998396" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptive Immunity ; Animals ; Anti-Bacterial Agents/pharmacology ; Bacterial Load ; Gram-Negative Bacteria/immunology/*physiology ; Gram-Positive Bacteria/immunology/*physiology ; Homeostasis ; Immunoglobulin A/analysis ; Intestinal Mucosa/immunology/*microbiology ; Intestine, Small/immunology/*microbiology ; Lectins, C-Type/physiology ; *Metagenome ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Myeloid Differentiation Factor 88/genetics/metabolism ; Proteins/*metabolism ; Symbiosis ; T-Lymphocytes, Helper-Inducer/immunology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 2006-08-26
    Beschreibung: The mammalian intestine harbors complex societies of beneficial bacteria that are maintained in the lumen with minimal penetration of mucosal surfaces. Microbial colonization of germ-free mice triggers epithelial expression of RegIIIgamma, a secreted C-type lectin. RegIIIgamma binds intestinal bacteria but lacks the complement recruitment domains present in other microbe-binding mammalian C-type lectins. We show that RegIIIgamma and its human counterpart, HIP/PAP, are directly antimicrobial proteins that bind their bacterial targets via interactions with peptidoglycan carbohydrate. We propose that these proteins represent an evolutionarily primitive form of lectin-mediated innate immunity, and that they reveal intestinal strategies for maintaining symbiotic host-microbial relationships.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2716667/" 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/PMC2716667/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cash, Heather L -- Whitham, Cecilia V -- Behrendt, Cassie L -- Hooper, Lora V -- R01 DK070855/DK/NIDDK NIH HHS/ -- R01 DK070855-01/DK/NIDDK NIH HHS/ -- T32-AI007520/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1126-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA. Lora.Hooper@UTSouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931762" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, Neoplasm/*metabolism/pharmacology ; Bacteria/growth & development/*immunology ; Biomarkers, Tumor/*metabolism/pharmacology ; Chitin/metabolism ; Colony Count, Microbial ; Germ-Free Life ; Gram-Positive Bacteria/immunology/metabolism ; Homeostasis ; Humans ; *Immunity, Innate ; Immunity, Mucosal ; Intestine, Small/*microbiology ; Lectins, C-Type/*metabolism ; Ligands ; Listeria monocytogenes/ultrastructure ; Mice ; Oligonucleotide Array Sequence Analysis ; Paneth Cells/immunology/*metabolism ; Peptidoglycan/chemistry/*metabolism ; Protein Structure, Tertiary ; Proteins/genetics/*metabolism/pharmacology ; Recombinant Proteins/metabolism ; Secretory Vesicles/metabolism ; Symbiosis
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
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