Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-6 (IL-6) plays a key role in inflammatory and immune responses in the host. In the present study, the IL-6 activity in urine from patients with various renal diseases was examined to elucidate the pathological and clinical significance of urinary IL-6. In patients with mesangial proliferative glomerulonephritis (mes-PGN) including, IgA nephropathy, the urinary IL-6 activity tended to increase with the progression of mesangial hypercellularity. In four patients with IgA nephropathy, urinary IL-6 activity increased markedly but transiently during episodes of acute exacerbation associated with upper respiratory tract infection. In addition, it was demonstrated that urine from patients with other types of PGN such as poststreptococcal acute glomerulonephritis and membrano-proliferative glomerulonephritis contained large quantities of IL-6. However, the levels of urinary IL-6 activity were almost within the normal range in non-proliferative glomerular diseases such as membranous nephropathy, minimal change nephrotic syndrome and lupus nephritis (WHO class I and V), non-glomerular bleeding and orthostatic proteinuria. It should be noted that a marked increase in urinary IL-6 was often observed in the patients with urinary tract infection. These results indicated that IL-6 in urine might be derived from various types of cells participating in inflammatory reactions not only in the renal parenchyma but also in the urinary tract.
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PMID:Detection and clinical usefulness of urinary interleukin-6 in the diseases of the kidney and the urinary tract. 142 4

We studied, using ELISA, 27 patients with IgA nephropathy to determine if levels of urinary interleukin-6 (IL-6) might reflect the disease activity. The levels of urinary IL-6 in patients with the advanced stage were significantly higher than those in patients with the mild stage of the disease or in healthy adults. The results showed a significant correlation between the levels of urinary IL-6 and the disease activity, i.e., levels of urinary cast and urinary protein. It was thus suggested that the measurement of urinary IL-6 is useful in evaluating the degree of glomerular injuries and/or prognosis in patients with IgA nephropathy.
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PMID:Urinary levels of interleukin-6 and disease activity in patients with IgA nephropathy. 181 12

IgA immune complex (IC) plays a crucial role in the pathogenesis of IgA nephropathy (IgAN). As IgA-IC is not itself cytotoxic, other mediators may be involved in the pathogenesis. In order to elucidate the mechanisms by which IgA-IC mediates renal injury in IgAN, the ability of IgA-IC to 'activate' cultured human mesangial cells (HMC) was studied. HMC were incubated with nephritogenic IgA-IC, containing a MOPC-315 plasmacytoma-derived IgA anti-dinitrophenyl (DNP) and DNP-conjugated bovine serum albumin. The cells showed morphological changes, an accelerated rate of proliferation, and increased production of interleukin-1 (IL-1), interleukin-6 (IL-6), platelet activating factor (PAF) and generation of superoxide anion. The enhancement of IL-1 and IL-6 mRNA expression in HMC incubated with IgA-IC was identified by dot blot analysis. Northern blot hybridization also demonstrated an augmented IL-6 mRNA expression in HMC treated with IgA-IC. These results suggest that nephritogenic IgA-IC may amplify the proliferation of HMC and the production of immune/chemical mediators and superoxide anion thereby resulting in the renal lesions of IgAN.
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PMID:Pathogenesis of IgA nephropathy: in vitro activation of human mesangial cells by IgA immune complex leads to cytokine secretion. 808 6

Using the intragastric ethanol infusion model of IgA nephropathy, we investigated the hypothesis that in this model mesangial changes commence prior to the deposition of IgA. We studied the two cellular components of the glomerular mesangium: the mononuclear phagocyte and the contractile mesangial cell. In the in vivo model, we observed a mononuclear phagocyte influx in the mesangium of alcoholic rats before the deposition of IgA. Using molecular techniques on cultured contractile mesangial cells, we demonstrated a threefold increase in interleukin-6 mRNA expression in contractile cells incubated with ethanol. These mesangial changes in the cellular composition, and in the autocrine cytokine system, suggest a direct role for ethanol in the pathogenesis of IgA nephropathy.
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PMID:Pathogenesis of IgA nephropathy in ethanol consumption: animal model and cell culture studies. 812 3

Mesangial proliferative glomerulonephritis (mesPGN) is histologically characterized by proliferation of mesangial cells (MC), suggesting the involvement of a growth factor for MC in the pathogenesis of mesPGN. We have previously shown that interleukin-6 (IL-6) induces proliferation of cultured rat mesangial cells, and urine samples from patients with IgA nephropathy contain high level of IL-6 activity. We have also demonstrated that transgenic mice carrying a human IL-6 genomic gene showed severe mesangial proliferation and matrix enlargement. Urinary samples of patients with lupus nephritis as well as IgA nephropathy contain significant IL-6 activity. Over a ten month follow-up, a positive correlation between the urinary IL-6 and pathological score was observed. Hence, measurement of urinary IL-6 can be used as a good indicator for monitoring IgA nephropathy and lupus nephritis. Using RT-PCR methods, IL-6 mRNA was detected in the glomeruli of renal biopsy specimens obtained from patients with IgA nephropathy and lupus nephritis.
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PMID:Role of interleukin-6 in the progression of mesangial proliferative glomerulonephritis. 846 29

IgA nephropathy, a form of mesangial glomerulonephritis, is associated with chronic ethanol ingestion in humans and in a rat model. We investigated the hypothesis that ethanol has a direct effect on a mesangial cell cytokine, interleukin-6 (IL-6). We measured IL-6 mRNA in cultured mesangial cells using a novel method, quantitative reverse transcription-polymerase chain reaction (Q-RT-PCR). Primers were used to amplify a 346-bp segment. To quantify the results, we generated an internal standard using site-directed mutagenesis which resulted in a restriction site for EcoRI, absent in target IL-6 cDNA. In the presence of the same primers, the mutated internal standard (exogenous template) amplifies with equal efficiency as the target IL-6 cDNA. Q-RT-PCR, using 250 ng of total RNA, showed that after ethanol incubation, IL-6 mRNA was 65 (+/-30) attomol, a 1.5-fold increase from 44 (+/-28) attomol in control cells. This study shows that in vitro, ethanol enhances IL-6 mRNA expression in rat mesangial cells.
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PMID:Quantitative reverse transcription polymerase chain reaction shows that ethanol enhances interleukin-6 mRNA expression in cultured mesangial cells. 872 8

A 16-year-old female with IgA nephropathy harboring histologically active lesions was treated with steroid mini-pulse therapy. Immunohistochemical examination revealed a diffuse distribution of interleukin-6 (IL-6) in the renal biopsy tissue. After treatment, her clinical factors and renal function improved, and renal biopsy showed reduced histological lesions and disappearance of the IL-6 distribution. Immunohistological studies of cytokines, such as IL-6, may be useful for evaluating the therapeutic effects in IgA nephropathy.
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PMID:Glomerular localization of interleukin-6 suppressed by steroid mini-pulse therapy in an IgA nephropathy patient. 892 46

Several studies have suggested that the measurement of urinary interleukin-6 (IL-6) is a helpful tool for diagnosis and monitoring the progression of glomerulonephritis. The aim of this study was to determine if IL-6 level might reflect the histological type of glomerular lesions. We performed a prospective study of 43 patients who underwent renal biopsy in our hospital. There were 35 male and 8 female patients with median age of 30.5 years (range 19-50). Included among these were 13 cases of IgA nephropathy, 11 cases of membranoproliferative glomerulonephritis, 6 cases of poststreptococcal glomerulonephritis, 6 cases of mesangial proliferative glomerulonephritis, 5 cases of membranous nephropathy and 2 cases of C3 nephritis. IL-6 was measured by ELISA (Lucernachem, Switzerland). IL-6 was not detected in the serum and rine of 15 healthy controls. IL-6 was elevated in the urine of 30 patients with different histological types of glomerular lesions (range 3.7 to 433.3 pg/ml) but was not detected in the urine of remaining 13 patients. The presence of IL-6 in the urine in absence of raised serum IL-6 suggests that urinary IL-6 was produced by the kidney. We have concluded that urinary IL-6 level can be considered as a marker of glomerulonephritis but not one that is very specific for any particular histological type of primary glomerulonephritis. Thus, the urinary IL-6 level is not a useful tool in the differential diagnosis of primary glomerulonephritis. We need further studies to determine whether urinary IL-6 level could by considered for monitoring of disease activity and therapy.
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PMID:[Serum and urinary interleukin-6 levels in patients with primary glomerulonephritis]. 910 25

In this study, we examined the receptors for the Fc portion of immunoglobulin A (IgA) (Fc alphaR) in the glomeruli as well as circulating polymorphonuclear leukocytes and monocytes at the mRNA level by reverse transcription-polymerase chain reaction (RT-PCR) assay and at the protein level by an immunohistochemistry/flow cytometry technique using a specific anti-Fc alphaR monoclonal antibody (My 43). Glomeruli were isolated from biopsy specimens of renal tissues from IgA nephropathy (IgAN; 20 cases) and non-IgA mesangial proliferative glomerulonephritis (PGN; 13 cases) patients, and from normal renal tissue specimens obtained from kidneys removed because of malignancies (five cases) applying the microdissection method. There was a relative increase in Fc alphaR in the circulating phagocytes from IgAN patients compared with those from PGN and healthy controls. Fc alphaR expression was present in approximately 40% of glomeruli samples from IgAN patients at the message levels. Fc alphaR-positive specimens were also strongly positive for expression of tumor necrosis factor-alpha, interleukin-1, and interleukin-6 mRNA. Specimens from PGN patients and healthy controls did not show any detectable Fc alphaR message. Serum IgA levels and severity of hematuria were significantly higher in patients with positive Fc alphaR expression. A message for Fc alphaR was detected in the tissues that were more damaged histologically. Our data suggest that there is some in vivo induction of glomerular Fc alphaR expression, possibly mediated by a synergistic stimulus from IgA and inflammatory cytokines, and the expressed receptor is likely to be involved in the disease process of IgAN.
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PMID:Glomerular Fc alphaR expression and disease activity in IgA nephropathy. 929 68

Various cytokines and growth factors may be involved in IgA nephropathy. To clarify whether interleukin-6 was a prognostic factor for this disease, we investigated interleukin-6 positivity of renal biopsy specimens and its relationship with the prognosis. The subjects were 90 patients with IgA nephropathy (42 males and 48 females with a median age of 32.7 +/- 13.8 years). Renal biopsy specimens were stained for interleukin-6 using an enzyme-antibody method. Fifty-two of 90 patients showed glomerular positivity for interleukin-6. Among the patients positive for interleukin-6, 24-hour urinary protein excretion and serum creatinine levels were significantly higher at the time of biopsy than in the patients without interleukin-6 positivity, while creatinine clearance was significantly lower. In the interleukin-6-positive patients without steroid therapy, serum creatinine increased significantly after 1 year (Deltas-Cr; 1.04 +/- 0.45 mg/dl) and creatinine clearance decreased significantly (DeltaCcr; -11.7 +/- 3.2 ml/min) compared to the interleukin-6-negative patients without steroid therapy. Steroid therapy improved 24-hour urinary protein excretion, serum creatinine, and creatinine clearance in the interleukin-6-positive patients, while these parameters worsened without steroid therapy. On the other hand, the IL-6-negative patients showed no differences of clinical parameters irrespective of the presence or absence of steroid therapy. In conclusion, glomerular interleukin-6 positivity may be a prognostic factor and an indicator of the need for steroid therapy in IgA nephropathy.
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PMID:Interleukin-6 localization and the prognosis of IgA nephropathy. 988 28


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