Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
PMID:Detection and clinical usefulness of urinary interleukin-6 in the diseases of the kidney and the urinary tract. 142 4

Interleukin-6 (IL-6) is a pleiotropic cytokine that has been postulated as playing a role in the pathogenesis of multiple myeloma, chronic autoimmune diseases, and alcoholic liver cirrhosis. We generated transgenic mice carrying a fusion between the mouse metallothionein-I (MT-I) gene promoter and the human IL-6 cDNA. MT-I/IL-6 transgenics express IL-6 constitutively in the liver and secrete the cytokine in the blood. They show initially activation of acute-phase response genes and accumulation of alpha 2- and beta-globulins in the plasma, which is followed by polyclonal hypergammaglobulinemia. MT-I/IL-6 transgenics die between 12 to 20 weeks of age. Histologic examination of transgenic animals at different ages and after necropsy showed, as expected from previous studies of IL-6 disregulation in vivo, an increase in the number of megakaryocytes in the spleen and bone marrow and, at later stages, IgG plasmacytosis in the spleen, lymph nodes, and thymus. However, no plasma cell infiltration was detected in other organs. The distinguishing feature of MT-I/IL-6 transgenics is the development of a progressive kidney pathology, in which the initial membranous glomerulonephritis is followed by focal glomerulosclerosis and finally by extensive tubular damage that reproduces the damage observed in patients at terminal stages of multiple myeloma (myeloma kidney). The pathogenetic role of IL-6 overproduction and of the resulting serum protein overload in the kidney damage is discussed.
 ...
PMID:Development of progressive kidney damage and myeloma kidney in interleukin-6 transgenic mice. 751 4

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.
 ...
PMID:[Serum and urinary interleukin-6 levels in patients with primary glomerulonephritis]. 910 25

Serum and urinary tumor necrosis factor-alpha (SeTNF and UTNF) and interleukin-6 (SeIL-6 and UIL-6) by ELISA method were determined in 99 patients with glomerulonephritis (GN): 13 with extracapillaris GN (ExGN), 38 with membranoproliferative GN (MPGN), 33 mesangial proliferative GN (MesPGN), 5 with focal segmental glomerulosclerosis (FSGS), 5 with membranous nephropathy (MN), 3 with minimal change nephropathy (MC) and in 32 healthy adults. The higher levels of Se TNF than those in the healthy were in 25 patients: in nearly all with ExGN, in 8 with MPGN and in single patients with other GN. In all patients with high SeTNF were many extra renal organs involvement. Measurable levels of UTNF were in 30 patients (30%) (in 12 with ExGN, 9 with MPGN, 7 with MesPGN, 1 with MN, and 1 with FSGS). Most patients with high SeTNF belonged to group I. The higher levels of SeIL-6 than those in healthy were in 17 patients belonging to group I, in which high SeIL-6 were in 3 patients with ExGN, 6 with MPGN, 3 with MesPGN, 2 with MN, and 3 with FSGS. Measurable urinary IL-6 levels were in 27 (27%) patients, mainly in group I, and in single patients in other groups. The majority of patients with ExGN and MPGN from group I and UIL-6 positive suffered from renal insufficiency and histologically had proliferative GN. We conclude that the elevation of TNF alpha and/or IL-6 in plasma may reflect a secondary consequence of immune cells activation while urinary TNF alpha and/or IL-6 may be secreted by activated glomerular cells. Thus, high levels of TNF alpha and/or IL-6 in serum of patients with GN and extra renal organs involvement, peculiary with infections, suggested antibiotics therapy, because infection may stimulated cytokines production and they are important in pathogenesis and progress of GN. High urinary levels of IL-6 and (or) TNF alpha in patients with proliferative GN suggest great disease activity and is useful in the evaluating of IS treatment.
 ...
PMID:[Tumor necrosis factor (TNF) and interleukin-6 (IL-6) in patients with glomerulonephritis]. 912 13

Membranous glomerulonephritis (MGN) remains the most common cause of adult-onset nephrotic syndrome in the world and up to 40% of untreated patients will progress to end-stage renal disease. Although the treatment of MGN with immunosuppressants or steroid hormones can attenuate the deterioration of renal function, numerous treatment-related complications have also been established. In this study, the ameliorative effects of arctiin, a natural compound isolated from the fruits of Arctium lappa, on rat glomerulonephritis induced by cationic bovine serum albumin (cBSA) were determined. After oral administration of arctiin (30, 60, 120 mg/kgd) for three weeks, the levels of serum creatinine (Scr) and blood urea nitrogen (BUN) and 24-h urine protein content markedly decreased, while endogenous creatinine clearance rate (ECcr) significantly increased. The parameters of renal lesion, hypercellularity, infiltration of polymorphonuclear leukocyte (PMN), fibrinoid necrosis, focal and segmental proliferation and interstitial infiltration, were reversed. In addition, we observed that arctiin evidently reduced the levels of malondialdehyde (MDA) and pro-inflammatory cytokines including interleukin-6 (IL-6) and tumor necrosis factor (TNF-alpha), suppressed nuclear factor-kappaB p65 (NF-kappaB) DNA binding activity, and enhanced superoxide dismutase (SOD) activity. These findings suggest that the ameliorative effects of arctiin on glomerulonephritis is carried out mainly by suppression of NF-kappaB activation and nuclear translocation and the decreases in the levels of these pro-inflammatory cytokines, while SOD is involved in the inhibitory pathway of NF-kappaB activation. Arctiin has favorable potency for the development of an inhibitory agent of NF-kappaB and further application to clinical treatment of glomerulonephritis, though clinical studies are required.
 ...
PMID:Ameliorative effects of arctiin from Arctium lappa on experimental glomerulonephritis in rats. 1952 15

Membranous glomerulonephritis (MGN) is viewed as an immune-mediated glomerular disease, with immunologic expression occurring in genetically susceptible persons. The cytokine interleukin-6 (IL-6) gene polymorphism is known to impair intracellular signaling pathways following adaptive immune response. Our study gauged the effects of IL-6 C-572G (rs1800796) single nucleotide polymorphism (SNP) on MGN among Taiwan's Han Chinese population, as analyzed in 265 controls and 106 MGN patients. Genotyping for IL-6 C-572G SNP was performed by restriction fragment length polymorphism assay. Data showed stark differences in genotype and allele frequency distributions at IL-6 C-572G SNP between MGN patients and controls (p = 1.6E-04 and 1.7E-04, respectively). People with C allele or with CC genotype at IL-6 C-572G SNP showed higher risk of MGN (odds ratio = 2.42 and 2.71, respectively; 95% confidence interval = 1.51-3.87 and 1.60-4.60, respectively). These point to IL-6 C-572G polymorphism as the underlying cause of MGN; polymorphism merits further investigation.
 ...
PMID:Effect of IL-6 C-572G polymorphism on idiopathic membranous nephropathy risk in a Han Chinese population. 2095 77