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  • 1
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    Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: The generation of cell-mediated immunity against many infectious pathogens involves the production of interleukin-12 (IL-12), a key signal of the innate immune system. Yet, for many pathogens, the molecules that induce IL-12 production by macrophages and the mechanisms by which they do so remain undefined. Here it is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs). Several lipoproteins stimulated TLR-dependent transcription of inducible nitric oxide synthase and the production of nitric oxide, a powerful microbicidal pathway. Activation of TLRs by microbial lipoproteins may initiate innate defense mechanisms against infectious pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brightbill, H D -- Libraty, D H -- Krutzik, S R -- Yang, R B -- Belisle, J T -- Bleharski, J R -- Maitland, M -- Norgard, M V -- Plevy, S E -- Smale, S T -- Brennan, P J -- Bloom, B R -- Godowski, P J -- Modlin, R L -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):732-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Howard Hughes Medical Institute, University of California Los Angeles School of Medicine, Los Anges, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/chemistry/*immunology/metabolism ; Cell Line ; *Drosophila Proteins ; Gene Expression Regulation ; Humans ; Interleukin-12/*biosynthesis/genetics ; Lipopolysaccharides/immunology ; Lipoproteins/chemistry/*immunology/metabolism ; Macrophages/*immunology/metabolism ; Membrane Glycoproteins/*metabolism ; Mice ; Monocytes/*immunology/metabolism ; Mycobacterium tuberculosis/*immunology ; NF-kappa B/biosynthesis ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase Type II ; Promoter Regions, Genetic ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; Toll-Like Receptors ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
    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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    Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-25
    Description: In innate immune responses, activation of Toll-like receptors (TLRs) triggers direct antimicrobial activity against intracellular bacteria, which in murine, but not human, monocytes and macrophages is mediated principally by nitric oxide. We report here that TLR activation of human macrophages up-regulated expression of the vitamin D receptor and the vitamin D-1-hydroxylase genes, leading to induction of the antimicrobial peptide cathelicidin and killing of intracellular Mycobacterium tuberculosis. We also observed that sera from African-American individuals, known to have increased susceptibility to tuberculosis, had low 25-hydroxyvitamin D and were inefficient in supporting cathelicidin messenger RNA induction. These data support a link between TLRs and vitamin D-mediated innate immunity and suggest that differences in ability of human populations to produce vitamin D may contribute to susceptibility to microbial infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Philip T -- Stenger, Steffen -- Li, Huiying -- Wenzel, Linda -- Tan, Belinda H -- Krutzik, Stephan R -- Ochoa, Maria Teresa -- Schauber, Jurgen -- Wu, Kent -- Meinken, Christoph -- Kamen, Diane L -- Wagner, Manfred -- Bals, Robert -- Steinmeyer, Andreas -- Zugel, Ulrich -- Gallo, Richard L -- Eisenberg, David -- Hewison, Martin -- Hollis, Bruce W -- Adams, John S -- Bloom, Barry R -- Modlin, Robert L -- AI052453/AI/NIAID NIH HHS/ -- AI22553/AI/NIAID NIH HHS/ -- AI47868/AI/NIAID NIH HHS/ -- AI48176/AI/NIAID NIH HHS/ -- AR45676/AR/NIAMS NIH HHS/ -- AR50626/AR/NIAMS NIH HHS/ -- HD043921/HD/NICHD NIH HHS/ -- K22 AI085025/AI/NIAID NIH HHS/ -- RR00425/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 24;311(5768):1770-3. Epub 2006 Feb 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Immunology, and Molecular Genetics, University of California at Los Angeles, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16497887" target="_blank"〉PubMed〈/a〉
    Keywords: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase/genetics ; African Americans ; Antimicrobial Cationic Peptides/biosynthesis/*genetics/metabolism ; Calcitriol/blood/*metabolism ; Cathelicidins ; Colony Count, Microbial ; Dendritic Cells/microbiology/physiology ; Disease Susceptibility ; Humans ; *Immunity, Innate ; Macrophages/immunology/microbiology/*physiology ; Monocytes/microbiology/*physiology ; Mycobacterium tuberculosis/*growth & development ; Oligonucleotide Array Sequence Analysis ; RNA, Messenger/genetics/metabolism ; Receptors, Calcitriol/genetics ; Steroid Hydroxylases/genetics ; Toll-Like Receptors/*physiology ; Tuberculosis/etiology/immunology ; Up-Regulation ; Vitamin D3 24-Hydroxylase
    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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  • 3
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    Type I interferon suppresses type II interferon-triggered human anti-mycobacterial responses (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-03-02
    Description: Type I interferons (IFN-alpha and IFN-beta) are important for protection against many viral infections, whereas type II interferon (IFN-gamma) is essential for host defense against some bacterial and parasitic pathogens. Study of IFN responses in human leprosy revealed an inverse correlation between IFN-beta and IFN-gamma gene expression programs. IFN-gamma and its downstream vitamin D-dependent antimicrobial genes were preferentially expressed in self-healing tuberculoid lesions and mediated antimicrobial activity against the pathogen Mycobacterium leprae in vitro. In contrast, IFN-beta and its downstream genes, including interleukin-10 (IL-10), were induced in monocytes by M. leprae in vitro and preferentially expressed in disseminated and progressive lepromatous lesions. The IFN-gamma-induced macrophage vitamin D-dependent antimicrobial peptide response was inhibited by IFN-beta and by IL-10, suggesting that the differential production of IFNs contributes to protection versus pathogenesis in some human bacterial infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653587/" 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/PMC3653587/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Teles, Rosane M B -- Graeber, Thomas G -- Krutzik, Stephan R -- Montoya, Dennis -- Schenk, Mirjam -- Lee, Delphine J -- Komisopoulou, Evangelia -- Kelly-Scumpia, Kindra -- Chun, Rene -- Iyer, Shankar S -- Sarno, Euzenir N -- Rea, Thomas H -- Hewison, Martin -- Adams, John S -- Popper, Stephen J -- Relman, David A -- Stenger, Steffen -- Bloom, Barry R -- Cheng, Genhong -- Modlin, Robert L -- P50 AR063020/AR/NIAMS NIH HHS/ -- R01 AI022553/AI/NIAID NIH HHS/ -- R01 AI047868/AI/NIAID NIH HHS/ -- R01 AI056154/AI/NIAID NIH HHS/ -- R01 AI082575/AI/NIAID NIH HHS/ -- R01 AR040312/AR/NIAMS NIH HHS/ -- R01 AR059126/AR/NIAMS NIH HHS/ -- T32 CA009120/CA/NCI NIH HHS/ -- UL1TR000124/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 22;339(6126):1448-53. doi: 10.1126/science.1233665. Epub 2013 Feb 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Dermatology, David Geffen School of Medicine at University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23449998" target="_blank"〉PubMed〈/a〉
    Keywords: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase/genetics/metabolism ; Antimicrobial Cationic Peptides/genetics/metabolism ; Humans ; Interferon-beta/genetics/*immunology/metabolism ; Interferon-gamma/genetics/*immunology/metabolism ; Interleukin-10/genetics/metabolism ; Leprosy, Lepromatous/genetics/*immunology/metabolism ; Leprosy, Tuberculoid/genetics/*immunology/metabolism ; Microbial Viability ; Monocytes/immunology/metabolism ; Mycobacterium leprae/*immunology/physiology ; RNA, Messenger/genetics/metabolism ; Receptors, Calcitriol/genetics/metabolism ; Transcriptome ; Tuberculosis/genetics/immunology ; Up-Regulation ; beta-Defensins/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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  • 4
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    T-cell cytokines differentially control human monocyte antimicrobial responses by regulating vitamin D metabolism (2010)
    National Academy of Sciences
    Details
    Publication Date: 2010-12-13
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 5
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    T-cell cytokines differentially control human monocyte antimicrobial responses by regulating vitamin D metabolism [Immunology] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-01-04
    Description: We investigated the mechanisms by which T-cell cytokines are able to influence the Toll-like receptor (TLR)-induced, vitamin D-dependent antimicrobial pathway in human monocytes. T-cell cytokines differentially influenced TLR2/1-induced expression of the antimicrobial peptides cathelicidin and DEFB4, being up-regulated by IFN-γ, down-regulated by IL-4, and unaffected by IL-17. The Th1 cytokine IFN-γ up-regulated TLR2/1 induction of 25-hydroxyvitamin D-1α-hydroxylase (i.e., CYP27B1), leading to enhanced bioconversion of 25-hydroxyvitamin D3 (25D3) to its active metabolite 1,25D3. In contrast, the Th2 cytokine IL-4, by itself and in combination with the TLR2/1 ligand, induced catabolism of 25D3 to the inactive metabolite 24,25D3, and was dependent on expression of vitamin D-24-hydroxylase (i.e., CYP24A1). Therefore, the ability of T-cell cytokines to differentially control monocyte vitamin D metabolism represents a mechanism by which cell-mediated immune responses can regulate innate immune mechanisms to defend against microbial pathogens.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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