Effect of high-dose methylprednisolone administration on immune functions in multiple sclerosis patients

被引:37
作者
Wandinger, KP
Wessel, K
Trillenberg, P
Heindl, N
Kirchner, H
机构
[1] Univ Lubeck, Sch Med, Inst Immunol & Transfus Med, D-23538 Lubeck, Germany
[2] Univ Lubeck, Sch Med, Dept Neurol, D-23538 Lubeck, Germany
来源
ACTA NEUROLOGICA SCANDINAVICA | 1998年 / 97卷 / 06期
关键词
multiple sclerosis; methylprednisolone; cytokines; immunoglobulins; interleukin-1; macrophage activation; NK cells;
D O I
10.1111/j.1600-0404.1998.tb05966.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objectives - To investigate the in vivo effect of corticosteroid pulse therapy on immunocompetent cells in 18 patients given methylprednisolone to treat an acute episode of MS. Material and methods - Blood was sampled before and after 3 days of methylprednisolone administration at doses of 1 g/day. Lymphocyte subtyping was performed and whole blood cell cultures were used to measure the cytokine producing capacity for interleukin-1 (IL-1), interleukin-2 (IL-2), interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha) and interferon-a (IFN-a). In addition, serum levels of the immunoglobulin classes IgG, IgA and IgM were determined. Results - Before treatment, production of IL-1 was significantly increased in MS patients as compared to healthy controls. After therapy, production of all cytokines was significantly decreased, whereas there were significant increases in the numbers of monocytes, neutrophils and T and B lymphocytes. Treatment had no effect on serum immunoglobulin levels. Conclusion - An important mechanism for the antiinflammatory effect of corticosteroids in MS results from a suppression of the activation of the peripheral immune compartment through inhibition of cytokine production and lymphocyte endothelial adhesiveness. (C) Munksgaard 1998.
引用
收藏
页码:359 / 365
页数:7
相关论文
共 63 条
[1]   LEUKOKINETIC STUDIES .4. TOTAL BLOOD, CIRCULATING AND MARGINAL GRANULOCYTE POOLS AND GRANULOCYTE TURNOVER RATE IN NORMAL SUBJECTS [J].
ATHENS, JW ;
WINTROBE, MM ;
ASHENBRUCKER, H ;
CARTWRIGHT, GE ;
MAUER, AM ;
HAAB, OP ;
RAAB, SO .
JOURNAL OF CLINICAL INVESTIGATION, 1961, 40 (06) :989-&
[2]   IMMUNOSUPPRESSION BY GLUCOCORTICOIDS - INHIBITION OF NF-KAPPA-B ACTIVITY THROUGH INDUCTION OF I-KAPPA-B SYNTHESIS [J].
AUPHAN, N ;
DIDONATO, JA ;
ROSETTE, C ;
HELMBERG, A ;
KARIN, M .
SCIENCE, 1995, 270 (5234) :286-290
[3]   REGULATION OF TRANSFORMING GROWTH FACTOR-BETA-1 GENE-EXPRESSION BY GLUCOCORTICOIDS IN NORMAL HUMAN LYMPHOCYTES-T [J].
AYANLARBATUMAN, O ;
FERRERO, AP ;
DIAZ, A ;
JIMENEZ, SA .
JOURNAL OF CLINICAL INVESTIGATION, 1991, 88 (05) :1574-1580
[4]   INCREASED PRODUCTION OF INTERFERON GAMMA AND TUMOR NECROSIS FACTOR PRECEDES CLINICAL MANIFESTATION IN MULTIPLE-SCLEROSIS - DO CYTOKINES TRIGGER OFF EXACERBATIONS [J].
BECK, J ;
RONDOT, P ;
CATINOT, L ;
FALCOFF, E ;
KIRCHNER, H ;
WIETZERBIN, J .
ACTA NEUROLOGICA SCANDINAVICA, 1988, 78 (04) :318-323
[5]   TGF-BETA-LIKE ACTIVITY PRODUCED DURING REGRESSION OF EXACERBATIONS IN MULTIPLE-SCLEROSIS [J].
BECK, J ;
RONDOT, P ;
JULLIEN, P ;
WIETZERBIN, J ;
LAWRENCE, DA .
ACTA NEUROLOGICA SCANDINAVICA, 1991, 84 (05) :452-455
[6]   THE EFFECT OF CORTICOSTEROIDS FOR ACUTE OPTIC NEURITIS ON THE SUBSEQUENT DEVELOPMENT OF MULTIPLE-SCLEROSIS [J].
BECK, RW ;
CLEARY, PA ;
TROBE, JD ;
KAUFMAN, DI ;
KUPERSMITH, MJ ;
PATY, DW ;
BROWN, CH .
NEW ENGLAND JOURNAL OF MEDICINE, 1993, 329 (24) :1764-1769
[7]  
BEVILACQUA MP, 1993, ANNU REV IMMUNOL, V11, P767, DOI 10.1146/annurev.iy.11.040193.004003
[8]   MACROCORTIN - A POLYPEPTIDE CAUSING THE ANTI-PHOSPHOLIPASE EFFECT OF GLUCOCORTICOIDS [J].
BLACKWELL, GJ ;
CARNUCCIO, R ;
DIROSA, M ;
FLOWER, RJ ;
PARENTE, L ;
PERSICO, P .
NATURE, 1980, 287 (5778) :147-149
[9]  
BLOEMENA E, 1990, CLIN EXP IMMUNOL, V80, P460
[10]   DEXAMETHASONE INHIBITS HUMAN INTERLEUKIN-2 BUT NOT INTERLEUKIN-2 RECEPTOR GENE-EXPRESSION INVITRO AT THE LEVEL OF NUCLEAR TRANSCRIPTION [J].
BOUMPAS, DT ;
ANASTASSIOU, ED ;
OLDER, SA ;
TSOKOS, GC ;
NELSON, DL ;
BALOW, JE .
JOURNAL OF CLINICAL INVESTIGATION, 1991, 87 (05) :1739-1747