TY - JOUR
T1 - Multiple sclerosis
T2 - pro- and anti-inflammatory cytokines and metalloproteinases are affected differentially by treatment with IFN-beta
AU - Ozenci, V
AU - Kouwenhoven, M
AU - Teleshova, N
AU - Pashenkov, M
AU - Fredrikson, S
AU - Link, H
PY - 2000/8/1
Y1 - 2000/8/1
N2 - Interferon-beta (IFN-beta) has a beneficial influence on the course of multiple sclerosis (MS) and has become standard treatment of this disease, though its mechanisms of action are incompletely understood. This study examines the effect of IFN-beta treatment on the cytokines IL-6, TNF-alpha, IFN-gamma and IL-10; the metalloproteinases MMP-3, -7 and -9 and the tissue inhibitor of metalloproteinase-1 (TIMP-1). IFN-beta treatment resulted in decreased numbers of mononuclear cells (MNC) secreting IL-6 and TNF-alpha and expressing mRNA of MMP-3 and MMP-9 compared to pretreatment levels. On the contrary, numbers of IL-10 secreting MNC and TIMP-1 mRNA expressing were augmented during IFN-beta therapy. Whether the down-regulatory effects on pro-inflammatory and upregulatory effects on anti-inflammatory molecules are a direct result of IFN-beta on the immune system or secondary to clinical stabilization of MS pathology induced by IFN-beta remains to be evaluated.
AB - Interferon-beta (IFN-beta) has a beneficial influence on the course of multiple sclerosis (MS) and has become standard treatment of this disease, though its mechanisms of action are incompletely understood. This study examines the effect of IFN-beta treatment on the cytokines IL-6, TNF-alpha, IFN-gamma and IL-10; the metalloproteinases MMP-3, -7 and -9 and the tissue inhibitor of metalloproteinase-1 (TIMP-1). IFN-beta treatment resulted in decreased numbers of mononuclear cells (MNC) secreting IL-6 and TNF-alpha and expressing mRNA of MMP-3 and MMP-9 compared to pretreatment levels. On the contrary, numbers of IL-10 secreting MNC and TIMP-1 mRNA expressing were augmented during IFN-beta therapy. Whether the down-regulatory effects on pro-inflammatory and upregulatory effects on anti-inflammatory molecules are a direct result of IFN-beta on the immune system or secondary to clinical stabilization of MS pathology induced by IFN-beta remains to be evaluated.
KW - Cells, Cultured
KW - Cytokines/metabolism
KW - Female
KW - Gene Expression Regulation/drug effects
KW - Gene Expression Regulation, Enzymologic/drug effects
KW - Humans
KW - In Situ Hybridization
KW - Inflammation/enzymology
KW - Interferon-beta/pharmacology
KW - Interferon-gamma/metabolism
KW - Interleukins/metabolism
KW - Leukocytes, Mononuclear/drug effects
KW - Longitudinal Studies
KW - Male
KW - Matrix Metalloproteinase 3/genetics
KW - Matrix Metalloproteinase 7/genetics
KW - Matrix Metalloproteinase 9/genetics
KW - Matrix Metalloproteinases/genetics
KW - Middle Aged
KW - Multiple Sclerosis/drug therapy
KW - RNA, Messenger/genetics
KW - Tissue Inhibitor of Metalloproteinase-1/genetics
KW - Tumor Necrosis Factor-alpha/metabolism
M3 - Article
C2 - 10900359
VL - 108
SP - 236
EP - 243
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
SN - 0165-5728
IS - 1-2
ER -