DEXAMETHASONE ATTENUATION OF CYTOKINE-MEDIATED ARTICULAR-CARTILAGE DEGRADATION IN EXPERIMENTAL LAPINE HAEMOPHILUS ARTHRITIS

被引:25
作者
JAFARI, HS
SAEZLLORENS, X
PARIS, M
RINDERKNECHT, S
FRIEDLAND, I
EHRETT, S
SEVERIEN, C
OLSEN, KD
BURNS, DK
HARPER, CF
LARK, MW
THONAR, EJMA
MCCRACKEN, GH
机构
[1] UNIV TEXAS,SW MED CTR,DEPT PEDIAT,5323 HARRY HINES BLVD,DALLAS,TX 75235
[2] MERCK INST THERAPEUT RES,RAHWAY,NJ 07065
[3] RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT BIOCHEM,CHICAGO,IL 60612
[4] RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT INTERNAL MED,CHICAGO,IL 60612
关键词
D O I
10.1093/infdis/168.5.1186
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The role of cytokines in the regulation of articular inflammation and cartilage degradation was evaluated in the rabbit model of Haemophilus influenzae type b arthritis. At 6 and 12 h after intraarticular infection, treatment with IB4 monoclonal antibody to the CD18 leukocyte receptor alone or in combination with dexamethasone resulted in significant reduction of synovial fluid (SF) neutrophil concentration. Treatment with dexamethasone alone was associated with lower SF concentrations of interleukin-1 (IL-1), tumor necrosis factor-alpha, and stromelysin than in other groups. At 24 h after infection, increased cartilage degradation was detected in untreated controls and in animals treated with IB4 alone or in combination with dexamethasone compared with those treated with dexamethasone alone. Multiple regression analyses indicated SF concentration of IL-1 and stromelysin as the significant predictors of cartilage degradation. These data suggest that IL-1 mediates cartilage degradation by regulation of metalloproteinases, such as stromelysin, during acute experimental bacterial arthritis.
引用
收藏
页码:1186 / 1193
页数:8
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