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Chemotactic and immunoregulatory properties of bone cells are modulated by endotoxin-stimulated lymphocytes.

Abstract

In our study, we explored the bidirectional communication via soluble factors between bone cells and endotoxin-stimulated splenic lymphocytes in an in vitro coculture model that mimics the inflammatory environment. Both the ability of lymphocytes to affect differentiation and immune properties of bone cells, osteoblasts (OBL) and osteoclasts (OCL), and of bone cells to modulate cytokine and activation profile of endotoxin-stimulated lymphocytes were tested. LPS-pulsed lymphocytes enhanced OCL but inhibited OBL differentiation and increased the RANKL/OPG ratio, and, at the same time, upregulated chemotactic properties of bone cells, specifically CCL2, CCL5, and CXCL10 in OCL and CCL5 and CXCL13 in OBL. In parallel, bone cells had immunosuppressive effects by downregulating the lymphocyte expression of interleukin (IL)-1, IL-6, TNF-α and co-stimulatory molecules. OCL stimulated the production of osteoclastogenic cytokine RANKL in T lymphocytes. The anti-inflammatory effect, especially of OBL, suggests a possible compensatory mechanism to limit the inflammatory reaction during infection.

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  • Publisher Full Text
  • Authors

    Cvija H, Kovacic N, Katavic V, Ivcevic S, Aguila HL, Marusic A, Grcevic D

    Institution

    Department of Physiology and Immunology, University of Zagreb School of Medicine, Salata 3, 10000 Zagreb, Croatia.

    Source

    Inflammation 35:5 2012 Oct pg 1618-31

    MeSH

    Animals
    Bone Marrow Cells
    Cell Differentiation
    Cells, Cultured
    Chemokine CCL2
    Chemokine CCL5
    Chemokine CXCL10
    Chemokine CXCL13
    Female
    Inflammation
    Interleukin-1
    Interleukin-6
    Lipopolysaccharides
    Lymphocyte Activation
    Lymphocytes
    Mice
    Mice, Inbred C57BL
    Osteoblasts
    Osteoclasts
    Osteoprotegerin
    RANK Ligand
    Tumor Necrosis Factor-alpha
    Up-Regulation

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    22699680