دورية أكاديمية
أعرض في EDS

S100A12 Is Part of the Antimicrobial Network against Mycobacterium leprae in Human Macrophages.

التفاصيل البيبلوغرافية
العنوان: S100A12 Is Part of the Antimicrobial Network against Mycobacterium leprae in Human Macrophages.
المؤلفون: Realegeno S; Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, United States of America., Kelly-Scumpia KM; Division of Dermatology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, United States of America., Dang AT; Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, United States of America., Lu J; Department of Molecular, Cell, and Developmental Biology, University of California, Los Angeles, Los Angeles, California, United States of America., Teles R; Division of Dermatology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, United States of America., Liu PT; UCLA/Orthopedic Hospital Department of Orthopedic Surgery, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, United States of America., Schenk M; Division of Dermatology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, United States of America., Lee EY; Department of Bioengineering, University of California, Los Angeles, Los Angeles, California, United States of America., Schmidt NW; Department of Bioengineering, University of California, Los Angeles, Los Angeles, California, United States of America., Wong GC; Department of Bioengineering, University of California, Los Angeles, Los Angeles, California, United States of America., Sarno EN; Leprosy Laboratory, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil., Rea TH; Department of Dermatology, University of Southern California School of Medicine, Los Angeles, California, United States of America., Ochoa MT; Department of Dermatology, University of Southern California School of Medicine, Los Angeles, California, United States of America., Pellegrini M; Department of Molecular, Cell, and Developmental Biology, University of California, Los Angeles, Los Angeles, California, United States of America., Modlin RL; Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, United States of America.; Division of Dermatology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, United States of America.
المصدر: PLoS pathogens [PLoS Pathog] 2016 Jun 29; Vol. 12 (6), pp. e1005705. Date of Electronic Publication: 2016 Jun 29 (Print Publication: 2016).
نوع المنشور: Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101238921 Publication Model: eCollection Cited Medium: Internet ISSN: 1553-7374 (Electronic) Linking ISSN: 15537366 NLM ISO Abbreviation: PLoS Pathog Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science, c2005-
مواضيع طبية MeSH: Leprosy/*immunology , Macrophages/*immunology , S100A12 Protein/*immunology, Flow Cytometry ; Fluorescent Antibody Technique ; Gene Expression Profiling ; Humans ; Macrophages/microbiology ; Mycobacterium Infections/immunology ; Mycobacterium leprae/immunology ; Mycobacterium tuberculosis/immunology ; Real-Time Polymerase Chain Reaction ; Transcriptome
مستخلص: Triggering antimicrobial mechanisms in macrophages infected with intracellular pathogens, such as mycobacteria, is critical to host defense against the infection. To uncover the unique and shared antimicrobial networks induced by the innate and adaptive immune systems, gene expression profiles generated by RNA sequencing (RNAseq) from human monocyte-derived macrophages (MDMs) activated with TLR2/1 ligand (TLR2/1L) or IFN-γ were analyzed. Weighed gene correlation network analysis identified modules of genes strongly correlated with TLR2/1L or IFN-γ that were linked by the "defense response" gene ontology term. The common TLR2/1L and IFN-γ inducible human macrophage host defense network contained 16 antimicrobial response genes, including S100A12, which was one of the most highly induced genes by TLR2/1L. There is limited information on the role of S100A12 in infectious disease, leading us to test the hypothesis that S100A12 contributes to host defense against mycobacterial infection in humans. We show that S100A12 is sufficient to directly kill Mycobacterium tuberculosis and Mycobacterium leprae. We also demonstrate that S100A12 is required for TLR2/1L and IFN-γ induced antimicrobial activity against M. leprae in infected macrophages. At the site of disease in leprosy, we found that S100A12 was more strongly expressed in skin lesions from tuberculoid leprosy (T-lep), the self-limiting form of the disease, compared to lepromatous leprosy (L-lep), the progressive form of the disease. These data suggest that S100A12 is part of an innate and adaptive inducible antimicrobial network that contributes to host defense against mycobacteria in infected macrophages.
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معلومات مُعتمدة: R01 AI022553 United States AI NIAID NIH HHS; R01 AI047868 United States AI NIAID NIH HHS; R37 AI047868 United States AI NIAID NIH HHS; UL1 TR000124 United States TR NCATS NIH HHS; R01 HL119068 United States HL NHLBI NIH HHS; P30 AI028697 United States AI NIAID NIH HHS; P50 AR063020 United States AR NIAMS NIH HHS; UL1 TR001881 United States TR NCATS NIH HHS; T32 GM008185 United States GM NIGMS NIH HHS; R01 AR040312 United States AR NIAMS NIH HHS
المشرفين على المادة: 0 (S100A12 Protein)
0 (S100A12 protein, human)
تواريخ الأحداث: Date Created: 20160630 Date Completed: 20170602 Latest Revision: 20230723
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC4927120
DOI: 10.1371/journal.ppat.1005705
PMID: 27355424
قاعدة البيانات: MEDLINE
الوصف
تدمد:1553-7374
DOI:10.1371/journal.ppat.1005705