دورية أكاديمية
أعرض في EDS

A complex proinflammatory cascade mediates the activation of HSCs upon LPS exposure in vivo.

التفاصيل البيبلوغرافية
العنوان: A complex proinflammatory cascade mediates the activation of HSCs upon LPS exposure in vivo.
المؤلفون: Demel UM; Division of Inflammatory Stress in Stem Cells, German Cancer Research Center (DKFZ), Heidelberg, Germany.; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGMBH), Heidelberg, Germany.; Department of Hematology, Oncology and Cancer Immunology, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany., Lutz R; Division of Inflammatory Stress in Stem Cells, German Cancer Research Center (DKFZ), Heidelberg, Germany.; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGMBH), Heidelberg, Germany.; Department of Hematology, Oncology and Rheumatology, University Hospital Heidelberg, Heidelberg, Germany., Sujer S; Division of Inflammatory Stress in Stem Cells, German Cancer Research Center (DKFZ), Heidelberg, Germany.; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGMBH), Heidelberg, Germany.; Faculty of Biosciences, University of Heidelberg, Heidelberg, Germany., Demerdash Y; Division of Inflammatory Stress in Stem Cells, German Cancer Research Center (DKFZ), Heidelberg, Germany.; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGMBH), Heidelberg, Germany.; Faculty of Biosciences, University of Heidelberg, Heidelberg, Germany., Sood S; Division of Inflammatory Stress in Stem Cells, German Cancer Research Center (DKFZ), Heidelberg, Germany.; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGMBH), Heidelberg, Germany.; Faculty of Biosciences, University of Heidelberg, Heidelberg, Germany., Grünschläger F; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGMBH), Heidelberg, Germany.; Faculty of Biosciences, University of Heidelberg, Heidelberg, Germany.; Division of Stem Cells and Cancer, German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance, Heidelberg, Germany., Kuck A; Division of Inflammatory Stress in Stem Cells, German Cancer Research Center (DKFZ), Heidelberg, Germany.; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGMBH), Heidelberg, Germany., Werner P; Division of Inflammatory Stress in Stem Cells, German Cancer Research Center (DKFZ), Heidelberg, Germany.; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGMBH), Heidelberg, Germany.; Faculty of Biosciences, University of Heidelberg, Heidelberg, Germany., Blaszkiewicz S; Division of Inflammatory Stress in Stem Cells, German Cancer Research Center (DKFZ), Heidelberg, Germany.; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGMBH), Heidelberg, Germany., Uckelmann HJ; Division of Inflammatory Stress in Stem Cells, German Cancer Research Center (DKFZ), Heidelberg, Germany.; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGMBH), Heidelberg, Germany.; Department of Pediatric Oncology, Dana-Farber Cancer Institute, and Division of Hematology/Oncology, Boston Children's Hospital and Harvard Medical School, Boston, MA., Haas S; Division of Inflammatory Stress in Stem Cells, German Cancer Research Center (DKFZ), Heidelberg, Germany.; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGMBH), Heidelberg, Germany.; Department of Hematology, Oncology and Cancer Immunology, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.; Division of Stem Cells and Cancer, German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance, Heidelberg, Germany.; German Cancer Consortium (DKTK), Heidelberg, Germany.; Berlin Institute of Health (BIH) at Charité-Universitätsmedizin Berlin, Berlin, Germany.; Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany; and.; Charité-Universitätsmedizin, Berlin, Germany., Essers MAG; Division of Inflammatory Stress in Stem Cells, German Cancer Research Center (DKFZ), Heidelberg, Germany.; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGMBH), Heidelberg, Germany.
المصدر: Blood advances [Blood Adv] 2022 Jun 14; Vol. 6 (11), pp. 3513-3528.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Society of Hematology Country of Publication: United States NLM ID: 101698425 Publication Model: Print Cited Medium: Internet ISSN: 2473-9537 (Electronic) Linking ISSN: 24739529 NLM ISO Abbreviation: Blood Adv Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Washington, DC : American Society of Hematology, [2016]-
مواضيع طبية MeSH: Lipopolysaccharides*/pharmacology , Toll-Like Receptor 4*/metabolism, Animals ; Cytokines/metabolism ; Hematopoiesis ; Hematopoietic Stem Cells/metabolism ; Mice
مستخلص: Infections are a key source of stress to the hematopoietic system. While infections consume short-lived innate immune cells, their recovery depends on quiescent hematopoietic stem cells (HSCs) with long-term self-renewal capacity. Both chronic inflammatory stress and bacterial infections compromise competitive HSC capacity and cause bone marrow (BM) failure. However, our understanding of how HSCs act during acute and contained infections remains incomplete. Here, we used advanced chimeric and genetic mouse models in combination with pharmacological interventions to dissect the complex nature of the acute systemic response of HSCs to lipopolysaccharide (LPS), a well-established model for inducing inflammatory stress. Acute LPS challenge transiently induced proliferation of quiescent HSCs in vivo. This response was not only mediated via direct LPS-TLR4 conjugation on HSCs but also involved indirect TLR4 signaling in CD115+ monocytic cells, inducing a complex proinflammatory cytokine cascade in BM. Downstream of LPS-TLR4 signaling, the combined action of proinflammatory cytokines such as interferon (IFN)α, IFNγ, tumor necrosis factor-α, interleukin (IL)-1α, IL-1β, and many others is required to mediate full HSC activation in vivo. Together, our study reveals detailed mechanistic insights into the interplay of proinflammatory cytokine-induced molecular pathways and cell types that jointly orchestrate the complex process of emergency hematopoiesis and HSC activation upon LPS exposure in vivo.
(© 2022 by The American Society of Hematology. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution. All other rights reserved.)
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المشرفين على المادة: 0 (Cytokines)
0 (Lipopolysaccharides)
0 (Toll-Like Receptor 4)
تواريخ الأحداث: Date Created: 20220412 Date Completed: 20220614 Latest Revision: 20220720
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC9198917
DOI: 10.1182/bloodadvances.2021006088
PMID: 35413096
قاعدة البيانات: MEDLINE
الوصف
تدمد:2473-9537
DOI:10.1182/bloodadvances.2021006088