Augmented Interleukin-18 Production by Peripheral Blood Monocytes in Patients with Minimal-Change Nephrotic Syndrome

2001 ◽  
Vol 21 (1) ◽  
pp. 20-27 ◽  
Author(s):  
Koichi Matsumoto ◽  
Katsuo Kanmatsuse
Keyword(s):  
Nephrotic Syndrome ◽  
Peripheral Blood ◽  
Minimal Change Nephrotic Syndrome ◽  
Minimal Change ◽  
Blood Monocytes ◽  
Interleukin 18 ◽  
Peripheral Blood Monocytes

Transcriptional and Post-Transcriptional Alterations of I κBα in Active Minimal-Change Nephrotic Syndrome

2001 ◽  
Vol 12 (8) ◽  
pp. 1648-1658 ◽  
Author(s):  
DJILLALI SAHALI ◽  
ANDRÉ PAWLAK ◽  
SABINE LE GOUVELLO ◽  
PHILIPPE LANG ◽  
ASTA VALANCIUTÉ ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Minimal Change Nephrotic Syndrome ◽  
Binding Activity ◽  
Minimal Change ◽  
Peripheral Blood Mononuclear ◽  
Nuclear Extracts ◽  
Blood Mononuclear Cells

Abstract. Minimal-change nephrotic syndrome (MCNS) is a renal disease characterized by heavy glomerular proteinuria and increased production of cytokines by immune cells. Because of the central role of nuclear factor-κB (NF-κB) in the regulation of cytokine expression, its activity during the relapse and remission phases of steroid-sensitive MCNS was analyzed. During relapse, nuclear extracts from peripheral blood mononuclear cells displayed high levels of NF-κB DNA-binding activity, consisting primarily of p50/RelA (p65) complexes. NF-κB p65 and IκBα proteins were barely detected or not detected in cytosolic fractions during relapse, in contrast to remission. The lack of expression of IκBα protein was associated with downregulation of IκBα mRNA and increases in the levels of the mRNA encoding the proteasome α2 subunit proteolytic pathway. In addition, inhibition of proteasome activity induced cytosolic accumulation of phosphorylated IκBα and significant reductions in the NF-κB binding activity in nuclear extracts from peripheral blood mononuclear cells from patients experiencing relapses. These results suggest that alterations in the NF-κB/IκBα regulatory feedback loop may contribute to the immunologic abnormalities that occur in steroidsensitive MCNS.

Characterization of Monocyte-Associated Factor V

1993 ◽  
Vol 70 (02) ◽  
pp. 273-280 ◽  
Author(s):  
Janos Kappelmayer ◽  
Satya P Kunapuli ◽  
Edward G Wyshock ◽  
Robert W Colman
Keyword(s):  
Monoclonal Antibody ◽  
Light Chain ◽  
Peripheral Blood ◽  
De Novo ◽  
Factor V ◽  
Blood Monocytes ◽  
De Novo Synthesis ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Peripheral Blood Monocytes

SummaryWe demonstrate that in addition to possessing binding sites for intact factor V (FV), unstimulated peripheral blood monocytes also express activated factor V (FVa) on their surfaces. FVa was identified on the monocyte surface by monoclonal antibody B38 recognizing FVa light chain and by human oligoclonal antibodies H1 (to FVa light chain) and H2 (to FVa heavy chain) using immunofluorescence microscopy and flow cytometry. On Western blots, partially cleaved FV could be identified as a 220 kDa band in lysates of monocytes. In addition to surface expression of FVa, monocytes also contain intracellular FV as detected only after permeabilization by Triton X-100 by monoclonal antibody B10 directed specifically to the Cl domain not present in FVa. We sought to determine whether the presence of FV in peripheral blood monocytes is a result of de novo synthesis.Using in situ hybridization, no FV mRNA could be detected in monocytes, while in parallel control studies, factor V mRNA was detectable in Hep G2 cells and CD18 mRNA in monocytes. In addition, using reverse transcriptase and the polymerase chain reaction, no FV mRNA was detected in mononuclear cells or in U937 cells, but mRNA for factor V was present in Hep G2 cells using the same techniques. These data suggest that FV is present in human monocytes, presumably acquired by binding of plasma FV, and that the presence of this critical coagulation factor is not due to de novo synthesis.

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