Superoxide release in juvenile systemic lupus erythematosus

被引:3
作者
Marini, Roberto [3 ]
Condino-Neto, Antonio [2 ,3 ]
Appenzeller, Simone [1 ]
Morcillo, Andre M. [2 ,3 ]
Costallat, Lilian T. L. [1 ]
机构
[1] Univ Estadual Campinas, Div Rheumatol, Dept Med, Fac Med Sci, BR-13087500 Campinas, SP, Brazil
[2] Univ Estadual Campinas, Ctr Invest Pediat, Dept Pediat, Fac Med Sci, BR-13087500 Campinas, SP, Brazil
[3] Univ Estadual Campinas, Med Rheumatol Unit, Fac Med Sci, BR-13087500 Campinas, SP, Brazil
基金
巴西圣保罗研究基金会;
关键词
Superoxide release; Systemic lupus erythematosus; RESPIRATORY BURST; FREE-RADICALS; NEUTROPHILS; LEUKOCYTES; MONOCYTES; CRITERIA; DNA;
D O I
10.1007/s00296-011-1918-7
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The objective of this study was to analyze the un-stimulated and stimulated release of superoxide anion (O-2 (-)) by granulocytes and monocytes in juvenile systemic lupus erythematosus (jSLE). The un-stimulated and phorbol myristate acetate (PMA, 30 nM)-induced O-2 (-)by granulocytes and monocytes were determined in six different times of incubation in patients with 23 jSLE and 28 controls. The analysis compared the jSLE group, which was classified into two subgroups by SLEDAI in one inactive subgroup (score < 3) (n = 13 patients) and one active subgroup (score a parts per thousand yen3) (n = 10 patients) to the same control group. At time of blood withdrawal, 13 (56.52%) had inactive and 10 (43.47%) patients had active SLE. jSLE patients' granulocytes and monocytes had always a lower un-stimulated O-2 (-) production when compared to controls. Stimulated granulocytes had an increased O-2 (-) production at baseline followed by a significant lower production at 60 min in jSLE when compared to controls. Stimulated monocytes had a similar O-2 (-) production among patients with jSLE and controls. The results suggest a defect in phagocytic function in jSLE. The significant higher release of O-2 (-) in the assays of the stimulated granulocytes, in the initial instances, the so-called respiratory burst, could be attributed to the inflammatory state of phagocytes.
引用
收藏
页码:1977 / 1983
页数:7
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