Abstract
The increased migration of peripheral blood mononuclear cells (PBMNCs) across a fibronectin (FN) matrix in response to the chemokines RANTES, MIP-1 alpha and MCP-1 is antagonized by interferon-beta-1b (IFN beta-1b). MCP-1 treatment of PBMNCs elevates their mRNA level and secretion of a matrix degrading enzyme, matrix metalloproteinase (MMP)-9, which is abrogated by IFN beta-1b. The clinical benefits of IFN beta-1b treatment in multiple sclerosis patients may in part be a result of this drug's ability to decrease the migration of PBMNCs in spite of a chemotactic gradient. Furthermore, the elevation of MMP-9 production by PBMNCs may be an important mechanism of action of chemokines.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Migration Inhibition*
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Cell Movement / drug effects
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Cell Movement / immunology
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Cell Separation
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Chemokine CCL2 / antagonists & inhibitors
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Chemokine CCL2 / pharmacology
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Chemokine CCL4
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Chemokine CCL5 / antagonists & inhibitors
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Chemokine CCL5 / pharmacology
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Chemokines / antagonists & inhibitors
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Chemokines / pharmacology*
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Collagenases / genetics
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Collagenases / metabolism
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Humans
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Interferon beta-1a
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Interferon beta-1b
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Interferon-beta / pharmacology*
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Leukocytes, Mononuclear / enzymology
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Leukocytes, Mononuclear / immunology*
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Leukocytes, Mononuclear / metabolism
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Macrophage Inflammatory Proteins / antagonists & inhibitors
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Macrophage Inflammatory Proteins / pharmacology
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Matrix Metalloproteinase 9
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Matrix Metalloproteinase Inhibitors*
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RNA, Messenger / antagonists & inhibitors
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RNA, Messenger / biosynthesis
Substances
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Chemokine CCL2
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Chemokine CCL4
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Chemokine CCL5
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Chemokines
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Macrophage Inflammatory Proteins
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Matrix Metalloproteinase Inhibitors
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RNA, Messenger
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Interferon beta-1b
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Interferon-beta
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Collagenases
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Matrix Metalloproteinase 9
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Interferon beta-1a