DIFFERENT CHEMOKINES ARE EXPRESSED IN HUMAN ARTHRITIC BONE BIOPSIES: IFN-γ AND IL-6 DIFFERENTLY MODULATE IL-8, MCP-1 AND RANTES PRODUCTION BY ARTHRITIC OSTEOBLASTS
Autor: | Andrea Facchini, Matilde Tschon, Anna Piacentini, S. Toneguzzi, Sandra Cristino, Gualtiero Gualtieri, Francesco Grassi, Gina Lisignoli |
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Rok vydání: | 2002 |
Předmět: |
Male
Chemokine medicine.medical_treatment Immunology Arthritis Biochemistry Bone and Bones Bone remodeling Interferon-gamma medicine Humans Immunology and Allergy Interleukin 8 Interleukin 6 Autocrine signalling Chemokine CCL5 Molecular Biology Chemokine CCL2 Aged Osteoblasts biology Interleukin-6 Chemistry Interleukin-8 Interleukin Hematology Middle Aged medicine.disease Immunohistochemistry Cytokine biology.protein Female |
Zdroj: | Cytokine. 20:231-238 |
ISSN: | 1043-4666 |
DOI: | 10.1006/cyto.2002.2006 |
Popis: | In the present study we analyse chemokine expression in the remodelling of subchondral bone in arthritis patients. Trabecular bone biopsies were tested by immunohistochemistry to identify interleukin (IL)-8, GRO-alpha, MCP-1, RANTES, MIP-1alpha and MIP-1beta expression. Subsequently, we evaluated by immunoassay the effect of interferon (IFN)-gamma and IL-6 on chemokine production by osteoarthritis (OA), rheumatoid arthritis (RA) and post-traumatic (PT) patients' isolated osteoblasts (OB). OB constitutively produced in situ IL-8, GRO-alpha, MCP-1, RANTES and MIP-1alpha. MIP-1beta was positive only in mononuclear cells. In RA many of these chemokines were also produced by mononuclear cells. IFN-gamma significantly down-regulated IL-8 and up-regulated MCP-1 produced by OB from all patients tested, whereas it did not affect the other chemokines analysed. Moreover, IFN-gamma reduced IL-1beta-stimulated IL-8 production but significantly increased both MCP-1 and RANTES. Interestingly, IL-6 significantly downregulated IFN-gamma-induced MCP-1 production, that was significantly lower in OA compared to RA patients. OB expressed chemokines both in vivo and in vitro suggesting that these cells are primary effectors in the bone capable of regulating autocrine/paracrine circuits that affect bone remodelling in these diseases. |
Databáze: | OpenAIRE |
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