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Prevention of endotoxin-induced systemic response by bone marrow-derived mesenchymal stem cells in mice.

Prevention of endotoxin-induced systemic response by bone marrow-derived mesenchymal stem cells in mice. Research Abstract Details 

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  • Prevention of endotoxin-induced systemic response by bone marrow-derived mesenchymal stem cells in mice. Abstract Text:

    jianguo xuJianguo Xu,charles r woodsCharles R Woods,ana l moraAna L Mora,robert joodiRobert Joodi,kenneth l brighamKenneth L Brigham,smita iyerSmita Iyer,mauricio rojasMauricio Rojas,

    Bone marrow-derived mesenchymal stem cells (BMDMSCs) appear to be important in repair of the chronic lung injury caused by bleomycin in mice. To determine effects of these BMDMSCs on an acute inflammatory response, we injected C57BL/6 mice intraperitoneally with 1 mg/kg endotoxin followed either by intravenous infusion of 5 x 10(5) BMDMSCs, the same number of lung fibroblasts, or an equal volume of normal saline solution. Lungs harvested 6, 24, and 48 h and 14 days after endotoxin showed that BMDMSC administration prevented endotoxin-induced lung inflammation, injury, and edema. Although we were able to detect donor cells in the lungs at 1 day after endotoxin, by 14 days no donor cells were detected. BMDMSC administration suppressed the endotoxin-induced increase in circulating proinflammatory cytokines without decreasing circulating levels of anti-inflammatory mediators. Ex vivo cocultures of BMDMSC and lung cells from endotoxemic animals demonstrated a bilateral conversation in which lung cells stimulated proliferation and migration of stem cells and suppressed proinflammatory cytokine production by lung cells. We conclude that BMDMSCs decrease both the systemic and local inflammatory responses induced by endotoxin. These effects do not require either lung engraftment or differentiation of the stem cells and are due at least in part to the production of stem cell chemoattractants by the lungs and to humoral and physical interactions between stem cells and lung cells. We speculate that mobilization of this population of BMDMSCs may be a general mechanism for modulating an acute inflammatory response.

    Prevention of endotoxin-induced systemic response by bone marrow-derived mesenchymal stem cells in mice. Publishing Authors By Initials

    j xuJ Xu,cr woodsCR Woods,al moraAL Mora,r joodiR Joodi,kl brighamKL Brigham,s iyerS Iyer,m rojasM Rojas,

    For similar proteins: membrane proteins: receptors, cell surface: receptors, immunologic: receptors, pattern recognition: toll-like receptors: toll-like receptor 4 research abstracts see: proteins: membrane proteins: receptors, cell surface: receptors, immunologic: receptors, pattern recognition: toll-like receptors: toll-like receptor 4 research

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    Prevention of endotoxin-induced systemic response by bone marrow-derived mesenchymal stem cells in mice. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: American journal of physiology. Lung cellular and

    VOLUME: 293

    Page Numbers: L131-41

    Journal Abbreviation: Am. J. Physiol. Lung Cell Mol.

    ISSN: 1040-0605

    DAY: 6

    MONTH: 04

    YEAR: 2007

    Prevention of endotoxin-induced systemic response by bone marrow-derived mesenchymal stem cells in mice. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901229

    Prevention of endotoxin-induced systemic response by bone marrow-derived mesenchymal stem cells in mice. Keywords Mesh Terms:

    KEYWORDS: Toll-Like Receptor 4

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Prevention of endotoxin-induced systemic response by bone marrow-derived mesenchymal stem cells in mice. Information

    Substance Name: Toll-Like Receptor 4

    Registry Number: 0

    Grant and Affiliation Information for Prevention of endotoxin-induced systemic response by bone marrow-derived mesenchymal stem cells in mice.

    AFFILIATION: Division of Pulmonary, Allergy and Critical Care Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: 5P01-HL-0669496-02

    ACRONYM: HL

    MEDLINETA: Am J Physiol Lung Cell Mol Phy

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    Number Hits: 0

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