The Experts below are selected from a list of 72 Experts worldwide ranked by ideXlab platform

Koichi Matsumoto - One of the best experts on this subject based on the ideXlab platform.

  • decreased release of il 10 by monocytes from patients with Lipoid Nephrosis
    Clinical and Experimental Immunology, 2008
    Co-Authors: Koichi Matsumoto
    Abstract:

    IL-10, a cross-regulatory cytokine produced by several cell types, including monocytes, is known to stimulate B cell growth and maturation and to inhibit cytokine production. In order to characterize further monocyte function in patients with Lipoid Nephrosis (LN), the release of IL-10 was measured in supernatants of cultured peripheral blood monocytes (PBM) that were obtained from LN patients and healthy controls. Spontaneous and lipopolysaccharide (LPS)-induced IL-10 release was decreased in patients with LN compared with those in normal controls and lower in LN patients with the nephrotic syndrome (NS) than in those without NS. In contrast, the values in IgA nephropathy (IgAN) patients with or without NS did not differ from normal subjects. There was a negative correlation between IL-10 concentration and the quantity of vascular permeability factor (VPF) released in LN patients. These imply that there is a relative deficit in IL-10 release in active LN, which suggests the possibility that inadequate release of IL-10 may lead to increased VPF activity in active LN patients and the measurements of IL-10 may be of value for monitoring kidney disease. The data provide the first detailed analysis of IL-10 in a group of patients with LN.

  • interleukin 12 upregulates the release of vascular permeability factor by peripheral blood mononuclear cells from patients with Lipoid Nephrosis
    Nephron, 1998
    Co-Authors: Koichi Matsumoto, Hiroyuki Ohi, Katsuo Kanmatsuse
    Abstract:

    The vascular permeability factor (VPF) is a lymphokine that has been shown to play a role in Lipoid Nephrosis (LN). Prior studies have shown that interleukin (IL) 12 promotes T helper type 1 differentiation and enhances production of T helper type 1 cytokines such as gamma interferon and IL-2. We, therefore, investigated the effects of recombinant human IL-12 on the release of VPF by peripheral blood mononuclear cells (PBMC) from LN patients. The VPF activity was measured according to the method of Ovary, with minor modifications. The goal of the present study was to examine the importance of IL-12 in concanavalin A induced VPF release in vitro. The levels of VPF were measured in a group of healthy subjects, LN patients with or without the nephrotic syndrome, and patients suffering from IgA nephropathy. There was a significantly increased concanavalin A induced release of VPF in LN and IgA nephropathy patients with nephrotic syndrome as compared with normal controls. Recombinant human IL-12 was found to enhance VPF release in a dose-dependent manner. Neutralization of endogenously produced IL-12 by anti-IL-12 antibody resulted in a decreased release of VPF by LN PBMC. These data indicate that endogenously produced IL-12 functions as a costimulatory molecule in vitro. Our data show that IL-12 can upregulate the release of VPF derived from LN PBMC. Thus IL-12 might be a potent adjuvant for inducing VPF. Therefore, IL-12 antagonists may interfere with newly initiated and ongoing VPF release associated with nephrotic syndrome.

  • interleukin 10 inhibits vascular permeability factor release by peripheral blood mononuclear cells in patients with Lipoid Nephrosis
    Nephron, 1997
    Co-Authors: Koichi Matsumoto
    Abstract:

    The effect of recombinant human interleukin 10 (IL-10) on the in vitro secretion of vascular permeability factor (VPF) of peripheral blood mononuclear cells (PBMC) was evaluated in patients with Lipoid Nephrosis (LN). Significantly increased spontaneous and concanavalin A (ConA) stimulated secretion of VPF was detected in PBMC cultures of LN patients with the nephrotic syndrome as compared with those of normal controls. In the present study, IL-10 inhibited the ConA-stimulated VPF secretion of PBMC in LN. A significant inhibitory effect of IL-10 was observed in cultures of PBMC from LN and IgA nephropathy patients as well as from normal persons. When both ConA and anti-IL-10 antibody were added together to the PBMC, a further increase in ConA-stimulated secretion of VPF occurred. These data suggest that IL-10 is a powerful inhibitor of the secretion of VPF in LN patients.

  • interleukin 10 and interleukin 13 synergize to inhibit vascular permeability factor release by peripheral blood mononuclear cells from patients with Lipoid Nephrosis
    Nephron, 1997
    Co-Authors: Koichi Matsumoto, Hiroyuki Ohi, Katsuo Kanmatsuse
    Abstract:

    It has been proposed that a vascular permeability factor (VPF) is involved in the pathogenesis of Lipoid Nephrosis (LN). There is now increasing evidence that interleukin 10 (IL-10) and interleukin 13 (IL-13) have regulatory effects on cytokine production by activated macrophages. These results prompted us to study the effects of recombinant human IL-10 and IL-13 on VPF secretion in LN. In the present study, we demonstrate that the regulatory cytokines IL-10 and IL-13 are potent inhibitors of the VPF activity of activated peripheral blood mononuclear cells. Each cytokine was found to suppress VPF secretion in a dose-dependent fashion. More importantly, the combination of the cytokines was found to give a potent synergistic suppression of VPF by concanavalin A activated peripheral blood mononuclear cells from patients with LN. When both anti-IL-10 and anti-IL-13 antibodies were added together to the peripheral blood mononuclear cells, a further increase of concanavalin A enhanced secretion of VPF occurred. These data establish IL-10 and IL-13 as potent inhibitors of VPF activity and suggest their utility in controlling deleterious VPF-mediated responses such as occur in LN patients with nephrotic syndrome.

Katsuo Kanmatsuse - One of the best experts on this subject based on the ideXlab platform.

  • interleukin 12 upregulates the release of vascular permeability factor by peripheral blood mononuclear cells from patients with Lipoid Nephrosis
    Nephron, 1998
    Co-Authors: Koichi Matsumoto, Hiroyuki Ohi, Katsuo Kanmatsuse
    Abstract:

    The vascular permeability factor (VPF) is a lymphokine that has been shown to play a role in Lipoid Nephrosis (LN). Prior studies have shown that interleukin (IL) 12 promotes T helper type 1 differentiation and enhances production of T helper type 1 cytokines such as gamma interferon and IL-2. We, therefore, investigated the effects of recombinant human IL-12 on the release of VPF by peripheral blood mononuclear cells (PBMC) from LN patients. The VPF activity was measured according to the method of Ovary, with minor modifications. The goal of the present study was to examine the importance of IL-12 in concanavalin A induced VPF release in vitro. The levels of VPF were measured in a group of healthy subjects, LN patients with or without the nephrotic syndrome, and patients suffering from IgA nephropathy. There was a significantly increased concanavalin A induced release of VPF in LN and IgA nephropathy patients with nephrotic syndrome as compared with normal controls. Recombinant human IL-12 was found to enhance VPF release in a dose-dependent manner. Neutralization of endogenously produced IL-12 by anti-IL-12 antibody resulted in a decreased release of VPF by LN PBMC. These data indicate that endogenously produced IL-12 functions as a costimulatory molecule in vitro. Our data show that IL-12 can upregulate the release of VPF derived from LN PBMC. Thus IL-12 might be a potent adjuvant for inducing VPF. Therefore, IL-12 antagonists may interfere with newly initiated and ongoing VPF release associated with nephrotic syndrome.

  • interleukin 10 and interleukin 13 synergize to inhibit vascular permeability factor release by peripheral blood mononuclear cells from patients with Lipoid Nephrosis
    Nephron, 1997
    Co-Authors: Koichi Matsumoto, Hiroyuki Ohi, Katsuo Kanmatsuse
    Abstract:

    It has been proposed that a vascular permeability factor (VPF) is involved in the pathogenesis of Lipoid Nephrosis (LN). There is now increasing evidence that interleukin 10 (IL-10) and interleukin 13 (IL-13) have regulatory effects on cytokine production by activated macrophages. These results prompted us to study the effects of recombinant human IL-10 and IL-13 on VPF secretion in LN. In the present study, we demonstrate that the regulatory cytokines IL-10 and IL-13 are potent inhibitors of the VPF activity of activated peripheral blood mononuclear cells. Each cytokine was found to suppress VPF secretion in a dose-dependent fashion. More importantly, the combination of the cytokines was found to give a potent synergistic suppression of VPF by concanavalin A activated peripheral blood mononuclear cells from patients with LN. When both anti-IL-10 and anti-IL-13 antibodies were added together to the peripheral blood mononuclear cells, a further increase of concanavalin A enhanced secretion of VPF occurred. These data establish IL-10 and IL-13 as potent inhibitors of VPF activity and suggest their utility in controlling deleterious VPF-mediated responses such as occur in LN patients with nephrotic syndrome.

Hiroyuki Ohi - One of the best experts on this subject based on the ideXlab platform.

  • interleukin 12 upregulates the release of vascular permeability factor by peripheral blood mononuclear cells from patients with Lipoid Nephrosis
    Nephron, 1998
    Co-Authors: Koichi Matsumoto, Hiroyuki Ohi, Katsuo Kanmatsuse
    Abstract:

    The vascular permeability factor (VPF) is a lymphokine that has been shown to play a role in Lipoid Nephrosis (LN). Prior studies have shown that interleukin (IL) 12 promotes T helper type 1 differentiation and enhances production of T helper type 1 cytokines such as gamma interferon and IL-2. We, therefore, investigated the effects of recombinant human IL-12 on the release of VPF by peripheral blood mononuclear cells (PBMC) from LN patients. The VPF activity was measured according to the method of Ovary, with minor modifications. The goal of the present study was to examine the importance of IL-12 in concanavalin A induced VPF release in vitro. The levels of VPF were measured in a group of healthy subjects, LN patients with or without the nephrotic syndrome, and patients suffering from IgA nephropathy. There was a significantly increased concanavalin A induced release of VPF in LN and IgA nephropathy patients with nephrotic syndrome as compared with normal controls. Recombinant human IL-12 was found to enhance VPF release in a dose-dependent manner. Neutralization of endogenously produced IL-12 by anti-IL-12 antibody resulted in a decreased release of VPF by LN PBMC. These data indicate that endogenously produced IL-12 functions as a costimulatory molecule in vitro. Our data show that IL-12 can upregulate the release of VPF derived from LN PBMC. Thus IL-12 might be a potent adjuvant for inducing VPF. Therefore, IL-12 antagonists may interfere with newly initiated and ongoing VPF release associated with nephrotic syndrome.

  • interleukin 10 and interleukin 13 synergize to inhibit vascular permeability factor release by peripheral blood mononuclear cells from patients with Lipoid Nephrosis
    Nephron, 1997
    Co-Authors: Koichi Matsumoto, Hiroyuki Ohi, Katsuo Kanmatsuse
    Abstract:

    It has been proposed that a vascular permeability factor (VPF) is involved in the pathogenesis of Lipoid Nephrosis (LN). There is now increasing evidence that interleukin 10 (IL-10) and interleukin 13 (IL-13) have regulatory effects on cytokine production by activated macrophages. These results prompted us to study the effects of recombinant human IL-10 and IL-13 on VPF secretion in LN. In the present study, we demonstrate that the regulatory cytokines IL-10 and IL-13 are potent inhibitors of the VPF activity of activated peripheral blood mononuclear cells. Each cytokine was found to suppress VPF secretion in a dose-dependent fashion. More importantly, the combination of the cytokines was found to give a potent synergistic suppression of VPF by concanavalin A activated peripheral blood mononuclear cells from patients with LN. When both anti-IL-10 and anti-IL-13 antibodies were added together to the peripheral blood mononuclear cells, a further increase of concanavalin A enhanced secretion of VPF occurred. These data establish IL-10 and IL-13 as potent inhibitors of VPF activity and suggest their utility in controlling deleterious VPF-mediated responses such as occur in LN patients with nephrotic syndrome.

Eduardo H Garin - One of the best experts on this subject based on the ideXlab platform.

  • cytokine mrna profile in Lipoid Nephrosis evidence for increased il 8 mrna stability
    Nephron, 2002
    Co-Authors: Paul F Laflam, Soichi Haraguchi, Eduardo H Garin
    Abstract:

    Background/Aims: Proteinuria in idiopathic minimal lesion nephrotic syndrome (IMLNS) is presumed to be due to the effect of circulating factors on glomerular permeability to plasma

  • anti interleukin 8 antibody abolishes effects of Lipoid Nephrosis cytokine
    Pediatric Nephrology, 1998
    Co-Authors: Eduardo H Garin, Paul F Laflam, Lamar Chandler
    Abstract:

    Supernatant factor from peripheral blood mononuclear cell (PBMC) cultures of idiopathic minimal lesion nephrotic syndrome (IMLNS) patients in relapse induces in vivo albuminuria and increases 35sulfate uptake by glomerular basement membrane (GBM) in rats. The purpose of this study was to evaluate the effect of anti-interleukin 8 (IL8) neutralizing antibody on the effects induced by the supernatant factor. Supernatant factor collected from six cultures of PBMC from IMLNS patients in relapse were combined and aliquotted into two samples. Anti-IL8 neutralizing antibody (750 ng) was added to one. Supernatant factor or supernatant factor and anti-IL8 antibody were infused for 5 days into the left renal artery of Wistar rats using an osmotic pump. On the last day of infusion, rats were injected with 35sulfate (1.0 mCi/200 g) intraperitoneally and killed after 8 h. Glomeruli were isolated and GBM obtained. There was a significant increase in 35sulfate uptake of the infused kidney (169 +/- 52 cpm/mg dry glomerular weight, mean +/- SEM) compared with the uptake seen in the contralateral kidney (116 +/- 41, P < 0.05) when the supernatant factor was infused alone. No significant differences in 35sulfate incorporation were seen between infused kidney (173 +/- 5) and contralateral kidney (190 +/- 49) when supernatant factor and anti-IL8 antibody were administered. A significant increase in albuminuria was seen on the last day of infusion (0.43 +/- 0.11 albumin/ creatinine ratio, mean +/- SEM) compared with the ratio prior to infusion of the supernatant factor alone (0.18 +/- 0.03, P <0.05). No significant differences in urinary albumin/creatinine ratios prior to and on the 5th day of infusion were seen when the supernatant factor was administered with anti-IL8 antibody. Supernatant factor effects were abolished by the addition of anti-IL8 neutralizing antibody, suggesting that the described effects are mediated by IL8.

  • effect of Lipoid Nephrosis cytokine on glomerular sulfated compounds and albuminuria
    Pediatric Nephrology, 1995
    Co-Authors: Eduardo H Garin
    Abstract:

    Supernatants from peripheral blood mononuclear cells cultures of 30 idiopathic, minimal lesion, nephrotic syndrome (IMLNS) patients in relapse and the same patients in remission were fractionated by gel filtration chromatography. Fractions eluting with carbonic anhydrase (29 kilodaltons) were infused for 5 days at the rate of 10 microliters/h into the left renal artery of Wistar rats using an Alzet osmotic pump. On the last day of infusion, rats were injected with 35sulfate (1.0 mCi/200 g) intraperitoneally and killed after 8 h. Glomeruli were isolated and glomerular basement membrane (GBM) obtained. There was a significant increase in 35sulfate uptake by GBM of the infused kidney (302 +/- 92 cpm/mg dry glomerular weight, mean +/- SEM) compared with the uptake seen in the contralateral kidney (157 +/- 36, P < 0.01) when the fraction from IMLNS patients in relapse was infused. No significant differences in 35sulfate incorporation were seen between infused kidney (166 +/- 41) and contralateral kidney (172 +/- 64) when the same fraction from patients in remission was administered. A significant increase in albuminuria was seen on the last day of infusion (14.2 +/- 1.0 mg/24 h, mean +/- SEM) when supernatant factor from IMLNS patients in relapse was used. No significant differences in urinary albumin excretion prior to and after infusion were seen when the same fraction from IMLNS patients in remission was administered. The in vivo infusion of supernatant factor from IMLNS patients in relapse increased the 35sulfate uptake by GBM and augmented albuminuria, suggesting that the factor may have pathogenic significance in the proteinuria of IMLNS.

Paul F Laflam - One of the best experts on this subject based on the ideXlab platform.

  • cytokine mrna profile in Lipoid Nephrosis evidence for increased il 8 mrna stability
    Nephron, 2002
    Co-Authors: Paul F Laflam, Soichi Haraguchi, Eduardo H Garin
    Abstract:

    Background/Aims: Proteinuria in idiopathic minimal lesion nephrotic syndrome (IMLNS) is presumed to be due to the effect of circulating factors on glomerular permeability to plasma

  • anti interleukin 8 antibody abolishes effects of Lipoid Nephrosis cytokine
    Pediatric Nephrology, 1998
    Co-Authors: Eduardo H Garin, Paul F Laflam, Lamar Chandler
    Abstract:

    Supernatant factor from peripheral blood mononuclear cell (PBMC) cultures of idiopathic minimal lesion nephrotic syndrome (IMLNS) patients in relapse induces in vivo albuminuria and increases 35sulfate uptake by glomerular basement membrane (GBM) in rats. The purpose of this study was to evaluate the effect of anti-interleukin 8 (IL8) neutralizing antibody on the effects induced by the supernatant factor. Supernatant factor collected from six cultures of PBMC from IMLNS patients in relapse were combined and aliquotted into two samples. Anti-IL8 neutralizing antibody (750 ng) was added to one. Supernatant factor or supernatant factor and anti-IL8 antibody were infused for 5 days into the left renal artery of Wistar rats using an osmotic pump. On the last day of infusion, rats were injected with 35sulfate (1.0 mCi/200 g) intraperitoneally and killed after 8 h. Glomeruli were isolated and GBM obtained. There was a significant increase in 35sulfate uptake of the infused kidney (169 +/- 52 cpm/mg dry glomerular weight, mean +/- SEM) compared with the uptake seen in the contralateral kidney (116 +/- 41, P < 0.05) when the supernatant factor was infused alone. No significant differences in 35sulfate incorporation were seen between infused kidney (173 +/- 5) and contralateral kidney (190 +/- 49) when supernatant factor and anti-IL8 antibody were administered. A significant increase in albuminuria was seen on the last day of infusion (0.43 +/- 0.11 albumin/ creatinine ratio, mean +/- SEM) compared with the ratio prior to infusion of the supernatant factor alone (0.18 +/- 0.03, P <0.05). No significant differences in urinary albumin/creatinine ratios prior to and on the 5th day of infusion were seen when the supernatant factor was administered with anti-IL8 antibody. Supernatant factor effects were abolished by the addition of anti-IL8 neutralizing antibody, suggesting that the described effects are mediated by IL8.