Macrophage inflammatory protein-1β and interleukin-8 associated with idiopathic steroid-sensitive nephrotic syndrome

被引:9
作者
Kanai, Takahiro [1 ]
Yamagata, Takanori [1 ]
Momoi, Mariko Y. [1 ]
机构
[1] Jichi Med Univ, Dept Pediat, Shimotsuke, Tochigi 3290498, Japan
关键词
children; idiopathic steroid-sensitive nephrotic syndrome; serum interleukin-8; serum macrophage inflammatory protein-1 beta; steroid treatment; GLOMERULAR BASEMENT-MEMBRANE; INCREASED PERMEABILITY; HEPARAN-SULFATE; TH1/TH2; BALANCE; CELL FUNCTION; LYMPHOCYTE-T; CYTOKINE; ALBUMINURIA; EXPRESSION; NEPHRITIS;
D O I
10.1111/j.1442-200X.2008.02759.x
中图分类号
R72 [儿科学];
学科分类号
100202 [儿科学];
摘要
Background: The cytokines associated with idiopathic steroid-sensitive nephrotic syndrome (ISSNS) have not been identified definitively, because previous studies had variable sampling and population heterogeneity. To clarify the cytokines involved, serum cytokine levels were measured using uniform sampling in a homogeneous population. Methods: Five children meeting the following criteria were included: (i) ISSNS; (ii) selectivity index < 0.1; (iii) paired sera obtained in the nephrotic phase before steroid treatment (STx; group A) and in the remission phase under STx (group B); (iv) no infection; and (v) no immunosuppressant. Control groups were as follows: group C, four children with ISSNS in the remission phase without STx; group D, five with normal urinalysis; group E, five with symptomatic secondary nephrotic syndrome before STx. Cytokine levels were measured using bead-based assay. Results: Serum macrophage inflammatory protein-1 beta (MIP-1 beta) levels were higher in group B compared to group A, and group C was lower than groups A and B. Serum interleukin-8 (IL-8) levels were higher in group A than in groups B and C, and groups B and C did not differ. With regard to both cytokine levels, there were no differences between groups C and D, and groups A and E. Conclusion: Serum MIP-1 beta and IL-8 are associated with the clinical status of ISSNS in children. A relationship between MIP-1 beta and ISSNS has not been previously reported. The mechanism by which MIP-1 beta and IL-8 affect ISSNS is unclear. Nevertheless, the present findings are an interesting starting point for further investigations into the pathophysiology of ISSNS in children.
引用
收藏
页码:443 / 447
页数:5
相关论文
共 30 条
[1]
Aarvak T, 1999, J IMMUNOL, V162, P1246
[2]
ALI AA, 1994, TRANSPLANTATION, V58, P849
[4]
A case of unfulfilled expectations. Cytokines in idiopathic minimal lesion nephrotic syndrome [J].
Araya, CE ;
Wasserfall, CH ;
Brusko, TM ;
Mu, W ;
Segal, MS ;
Johnson, RJ ;
Garin, EH .
PEDIATRIC NEPHROLOGY, 2006, 21 (05) :603-610
[5]
Chensue SW, 1996, J IMMUNOL, V157, P4602
[6]
Daniel V, 1997, CLIN NEPHROL, V47, P289
[7]
2 TYPES OF MOUSE T-HELPER CELL .4. TH2 CLONES SECRETE A FACTOR THAT INHIBITS CYTOKINE PRODUCTION BY TH1 CLONES [J].
FIORENTINO, DF ;
BOND, MW ;
MOSMANN, TR .
JOURNAL OF EXPERIMENTAL MEDICINE, 1989, 170 (06) :2081-2095
[8]
IL-8 PRODUCTION BY PERIPHERAL-BLOOD MONONUCLEAR-CELLS IN NEPHROTIC PATIENTS [J].
GARIN, EH ;
BLANCHARD, DK ;
MATSUSHIMA, K ;
DJEU, JY .
KIDNEY INTERNATIONAL, 1994, 45 (05) :1311-1317
[9]
Effect of interleukin-8 on glomerular sulfated compounds and albuminuria [J].
Garin, EH ;
West, L ;
Zheng, W .
PEDIATRIC NEPHROLOGY, 1997, 11 (03) :274-279
[10]
CLONING OF A T-CELL GROWTH-FACTOR THAT INTERACTS WITH THE BETA-CHAIN OF THE INTERLEUKIN-2 RECEPTOR [J].
GRABSTEIN, KH ;
EISENMAN, J ;
SHANEBECK, K ;
RAUCH, C ;
SRINIVASAN, S ;
FUNG, V ;
BEERS, C ;
RICHARDSON, J ;
SCHOENBORN, MA ;
AHDIEH, M ;
JOHNSON, L ;
ALDERSON, MR ;
WATSON, JD ;
ANDERSON, DM ;
GIRI, JG .
SCIENCE, 1994, 264 (5161) :965-968