Up-regulation of interleukin-2 mRNA in children with idiopathic nephrotic syndrome

被引:37
作者
Shimoyama, H
Nakajima, M
Naka, H
Maruhashi, Y
Akazawa, H
Ueda, T
Nishiguchi, M
Yamoto, Y
Kamitsuji, H
Yoshioka, A
机构
[1] Nara Med Univ, Dept Pediat, Kashihara, Nara 6348522, Japan
[2] Nara Prefectural Nara Hosp, Dept Pediat, Nara, Japan
关键词
cytokines; interleukin-2; idiopathic nephrotic syndrome; real-time PCR assay; mRNA;
D O I
10.1007/s00467-004-1569-y
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
The current hypothesis for the pathogenesis of childhood idiopathic nephrotic syndrome (INS) favors the involvement of a T cell-mediated immune response. Various cytokines derived from T cells may play a critical role in INS. Previous studies have measured serum or urine cytokine levels and suggest an imbalance of the T cell-mediated immune response. To elucidate the true profile of T cell-derived cytokines, we determined interleukin (IL)-2, interferon (IFN)-gamma, IL-4, IL-10, and tumor necrosis factor (TNF)-alpha mRNA expression in children with INS. We collected mRNA from peripheral blood mononuclear cells together with plasma and urine from nine children in the acute and remission phases of INS. Expression of IL-2, IFN-gamma, IL-4, IL-10, and TNF-alpha mRNA was determined by a quantitative real-time PCR assay. Plasma and urine cytokine concentrations were measured using a specific enzyme-linked immunosorbent assay. These data were compared between the acute and remission phase in the same patients. The IL-2 mRNA levels were significantly higher in the acute phase than in the remission phase, whilst no significant difference was found in the other cytokines investigated. There was no significant difference in the plasma and urine cytokine concentrations between the acute and remission phase. Our results indicate increased expression of IL-2 mRNA in the acute phase of INS, suggesting that IL-2, at least in part, might be involved in the pathophysiology of childhood INS.
引用
收藏
页码:1115 / 1121
页数:7
相关论文
共 26 条
[2]   Effects of glucocorticoids and cyclosporine on IL-2 and IκBα mRNA expression in human peripheral blood mononuclear cells [J].
Briggs, WA ;
Han, SH ;
Miyakawa, H ;
Burdick, JF ;
Kwon, HM .
JOURNAL OF CLINICAL PHARMACOLOGY, 1999, 39 (02) :119-124
[3]   THE TREATMENT OF MINIMAL CHANGE NEPHROTIC SYNDROME - LESSONS LEARNED FROM MULTICENTER COOPERATIVE STUDIES [J].
BRODEHL, J .
EUROPEAN JOURNAL OF PEDIATRICS, 1991, 150 (06) :380-387
[4]   INCREASE OF TUMOR-NECROSIS-FACTOR-ALPHA SYNTHESIS AND GENE-EXPRESSION IN PERIPHERAL-BLOOD MONONUCLEAR-CELLS OF CHILDREN WITH IDIOPATHIC NEPHROTIC SYNDROME [J].
BUSTOS, C ;
GONZALEZ, E ;
MULEY, R ;
ALONSO, JL ;
EGIDO, J .
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 1994, 24 (12) :799-805
[5]   Up-regulation of interleukin-4 and CD23/FcεRII in minimal change nephrotic syndrome [J].
Cho, BS ;
Yoon, SR ;
Jang, JY ;
Pyun, KH ;
Lee, CE .
PEDIATRIC NEPHROLOGY, 1999, 13 (03) :199-204
[6]  
Daniel V, 1997, CLIN NEPHROL, V47, P289
[7]   Dominant T cells in idiopathic nephrotic syndrome of childhood [J].
Frank, C ;
Herrmann, M ;
Fernandez, S ;
Dirnecker, D ;
Böswald, M ;
Kolowos, W ;
Ruder, H ;
Haas, JP .
KIDNEY INTERNATIONAL, 2000, 57 (02) :510-517
[8]   RECOMBINANT INTERLEUKIN-2 ALONE DID NOT INDUCE PROTEINURIA WITH CHANGES IN ANIONIC SITES OF THE GLOMERULAR-BASEMENT-MEMBRANE IN RATS [J].
FUJIMOTO, S ;
YAMAMOTO, Y ;
HISANAGA, S ;
YOKOTA, N ;
ETO, T .
NEPHRON, 1992, 61 (01) :117-118
[9]   DECREASED PRODUCTION AND RESPONSIVENESS OF INTERLEUKIN-2 IN LYMPHOCYTES OF PATIENTS WITH NEPHROTIC SYNDROME [J].
HINOSHITA, F ;
NOMA, T ;
TOMURA, S ;
SHIIGAI, T ;
YATA, J .
NEPHRON, 1990, 54 (02) :122-126
[10]   Clinical impact of cyclosporine cellular pharmacodynamics in minimal change nephrotic syndrome [J].
Hirano, T ;
Akashi, T ;
Keira, T ;
Oka, K ;
Ihoya, N ;
Yoshida, M .
CLINICAL PHARMACOLOGY & THERAPEUTICS, 2000, 68 (05) :532-540