Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-8 (IL-8) has been reported to be released by activated peritoneal macrophages (PMs) and a variety of other cell types, and it exhibits potent chemotactic activity for polymorphonuclear cells (PMNs). We have previously shown that IL-8 is detectable in the drain dialysate of uremic patients on continuous ambulatory peritoneal dialysis (CAPD) during peritonitis. The levels of IL-8 in infected drain dialysate caused by different microorganisms were variable. In this study, we evaluated the gene expression and release of IL-8 by PMs and PMNs during peritonitis caused by Staphylococcus aureus in uremic patients on CAPD. IL-8 levels were variable in the drain dialysate at the different episodes of peritonitis, even in the same patient. The IL-8 levels were highly correlated with PMN count in drain dialysate (r = 0.9919, p < 0.001). PMs and PMNs obtained from drain dialysate at the onset of peritonitis increased mRNA expression for IL-8 and the amount of IL-8 mRNA from drainage cells was also highly correlated with PMN count. In contrast, cells isolated from drain dialysate without peritonitis failed to express mRNA for IL-8. These data suggest that increased expression of IL-8 may be a feature of peritonitis. The levels of IL-8 during peritonitis were not only related to the etiological microorganism but also to other unknown factor(s).
Nephron 1994
PMID:Gene expression and release of interleukin-8 by peritoneal macrophages and polymorphonuclear leukocytes during peritonitis in uremic patients on continuous ambulatory peritoneal dialysis. 787 Feb 28

Urine and serum concentrations of interleukin (IL)-6 and IL-8 were determined in 43 women with acute pyelonephritis caused by Escherichia coli. Urine and serum samples were also collected 2 weeks after the infection and during a subsequent episode of cystitis (n = 8) or asymptomatic bacteriuria (n = 8). Concentrations of IL-6 and IL-8 were related to the expression of 5 virulence markers of E. coli and glomerular filtration rate (GFR) after pyelonephritis. Patients with acute pyelonephritis had elevated urine and serum IL-6 and IL-8 levels as compared to 37 healthy women (IL-6: p < 0.001 in both cases, and IL-8: p < 0.001 in both cases). Patients infected with E. coli producing hemolysin and/or cytotoxic necrotizing factor (CNF) had significantly higher IL-6 levels in serum during acute pyelonephritis as compared to patients infected with strains without the ability to produce these factors (p = 0.0025 and p = 0.0154, respectively). Patients who had high concentrations of IL-8 in urine during acute pyelonephritis had lower GFR at follow-up as compared to patients with lower levels of IL-8 in urine (r = -0.48, p = 0.0123). In conclusion, acute pyelonephritis is accompanied by elevated urinary and serum IL-6 and IL-8 levels. Bacteria producing hemolysin and CNF seem to induce higher concentrations of IL-6 in serum. The secretion of IL-8 from renal cells may participate in the initiation and maintenance of renal inflammation which in turn may influence renal function.
Nephron 1994
PMID:Interleukin-6 and interleukin-8 in serum and urine in patients with acute pyelonephritis in relation to bacterial-virulence-associated traits and renal function. 791 3

In this study, we investigated whether peritoneal dialysate interleukin-6 (IL-6) and IL-8 levels were elevated during peritonitis in continuous ambulatory peritoneal dialysis (CAPD) patients, with special reference to the high peritonitis occurrence (HPO) group. Serial measurements of IL-6 and IL-8 levels in dialysate before, during and after resolution of peritonitis were done in 13 CAPD patients with 15 episodes of peritonitis. Based on the peritonitis occurrence, 7 patients were assigned to the low peritonitis occurrence (LPO) and 6 patients to the HPO group. Marked elevation of IL-6 and IL-8 in drain dialysate occurred in the early period of peritonitis especially on the first 2 days in both groups. However, there were no significant differences between the groups in the levels of IL-6 and IL-8 in drain dialysate on the first day of peritonitis. However, the disappearance of peritoneal dialysate IL-8 level was faster in the LPO than in the HPO group. The decrease in IL-8 levels during peritonitis was faster than that of IL-6. Marked elevation of IL-6 and IL-8 in drain dialysate was found in the patient with peritonitis caused by Staphylococcus epidermidis and mixed gram-negative bacilli. Therefore, we hypothesize that when peritonitis occurs too frequently in a short period in the HPO group, more IL-6 and IL-8 have been produced in the peritoneum contributing to the ongoing peritoneal injury and/or fibrosis.
Nephron 1993
PMID:Serial changes of interleukin-6 and interleukin-8 levels in drain dialysate of uremic patients with continuous ambulatory peritoneal dialysis during peritonitis. 845 75

We have previously shown that lymphocytes from idiopathic minimal-lesion nephrotic patients produce a lymphokine (supernatant factor) that increases the 35sulfate uptake in the glomerular basement membrane (GBM). The purpose of this report was to further characterize the supernatant factor by studying the effects of interleukins (IL) 2-4, 6, and 8, granulocyte-macrophage colony stimulating factor, and tumor necrosis factor on the 35sulfate incorporation by rat glomeruli in vitro. A significant increase in GBM 35sulfate uptake was only seen when the glomeruli were cultured with the addition of IL-8 as compared with control cultures: 10.8 +/- (SEM) 1.7 and 7.9 +/- 1.4 cpm/micrograms GBM protein, respectively (p < 0.005). IL-8 reproduces the effect of the reported supernatant factor on the GBM 35sulfate uptake. Because IL-8 was detected in the supernatant of peripheral mononuclear cell cultures from idiopathic minimal-lesion nephrotic syndrome patients in relapse and because the increased GBM 35sulfate incorporation induced by the supernatant factor has been abolished by the addition to the culture media of anti-IL-8 neutralizing antibodies, we postulate that IL-8 is the previously described supernatant factor.
Nephron 1995
PMID:Effect of lymphokines on 35sulfate uptake by the glomerular basement membrane. 858 25

The biocompatibility of a 1.1% amino acid-containing peritoneal dialysis fluid (AA-PDF) was compared to that of a 2.27% glucose-based peritoneal dialysis fluid (G-PDF). Peritoneal macrophages (PMO), isolated from the peritoneal dialysis (PD) effluents of 10 chronic ambulatory PD patients, were tested for their phagocytosis capacity and peak chemiluminescence response. A subset of PMO was cultured for 24 h with and without lipopolysaccharide (LPS) to study the release of interleukin-1 beta (IL-1 beta) and 8 (IL-8). As control, the interleukin release by blood monocytes of healthy donors was tested. The opsonic activity of the PD effluent was tested as well. Compared to PMO isolated from G-PDF, PMO from AA-PDF showed a significantly better phagocytosis capacity. There was no difference in the peak chemiluminescence response between PMO from AA-PDF and G-PDF. The release of IL-1 beta by unstimulated PMO isolated from the two fluids did not differ. Compared to control monocytes, however, PMO from both fluids showed a considerable spontaneous release of IL-1 beta. When stimulated with LPS, IL-1 beta production by PMO from G-PDF exceeded that of PMO from AA-PDF (p < 0.002). The release of IL-8 by PMO from G-PDF was significantly higher in comparison with PMO from AA-PDF, both spontaneously and after stimulation with LPS (p < 0.02). The opsonic activity of undiluted and to 75% diluted effluents was significantly higher for G-PDF than for AA-PDF (p < 0.01). Thus, compared to the regularly used G-PDF, the phagocytosis capacity as measure for PMO function seems to be better preserved after in vivo exposure to AA-PDF. In addition, the higher release of IL-1 beta and IL-8 by PMO isolated from G-PDF suggests a stronger intra-abdominal activation of PMO, with G-PDF acting as a chemical inflammatory agent. Whether the lower opsonic activity of the AA-PDF is more important for biocompatibility than the other parameters is not clear. Therefore, it is concluded that, although macrophage function is better preserved, it is not proven that the 1.1% AA-PDF studied has an improved biocompatibility compared to 2.27% G-PDF.
Nephron 1996
PMID:Biocompatibility of a 1.1% amino acid-containing peritoneal dialysis fluid compared to a 2.27% glucose-based peritoneal dialysis fluid. 888 16

In this study we have examined the effects of recombinant human interleukin (IL)-13 on peripheral blood monocytes (PBM) from patients with IgA nephropathy (IgAN). Significantly increased spontaneous and lipopolysaccharide (LPS)-stimulated secretion of tumor necrosis factor-alpha (TNF) and IL-8 was determined in PBM cultures of IgAN patients compared to those of normal controls. In the present study, IL-13 inhibited the spontaneous as well as the LPS-stimulated cytokine secretion of PBM in IgAN. Significant inhibitory effect of IL-13 was observed in cultures of PBM from IgAN patients as well as from normal persons. When both LPS and anti-IL-13 antibody were added together to the PBM, a further increase of LPS-enhanced secretion of cytokines occurred. Taken together, these results indicate that IL-13 down-regulates the secretion of TNF and IL-8 from IgAN PBM.
Nephron 1997
PMID:Interleukin-13 inhibits cytokine secretion by blood monocytes from patients with IgA nephropathy. 906 51

Tubulointerstitial nephritis is a less frequently recognized but important complication of systemic lupus erythematosus. We have investigated the cytokine beta2-microglobulin (beta2M) and Tamm-Horsfall glycoprotein (THG) excretions in the urine of systemic lupus erythematosus patients to identify indices for evaluation of tubulointerstitial inflammation in lupus nephritis (LN). Daily urine was collected from 15 patients with active LN, from 12 patients with inactive LN, and from 17 normal subjects. The amounts of soluble interleukin (IL) 2 receptor, IL-6, IL-8, beta2M, and THG in urine were measured. Beta2M and THG were regarded as indicators of proximal and distal renal tubule function, respectively. The urinary excretions of IL-6 and IL-8 were significantly higher in patients with active LN than in those with inactive LN and in normal individuals. The excretion of soluble IL-2 receptor in all three groups of subjects was not significantly different. On the other hand, the excretion of beta2M in patients with LN was significantly higher than that in normal individuals. The excretion of beta2M in patients with active or inactive LN was not significantly different. The THG excretion was lower in patients with active LN and tubulointerstitial inflammation as compared with patients with inactive LN or normal individuals. Six patients underwent pulse cyclophosphamide therapy during the course of experiments. Five of them showed a decrease in IL-8 and IL-6 excretions in urine after the treatment. The excretions of beta2M and THG in urine, in addition to IL-6 and IL-8, can reflect the renal inflammatory activity in patients with lupus tubulointerstitial nephritis as well as in those having lupus glomerulonephritis.
Nephron 2000 Jul
PMID:Increased excretions of beta2-microglobulin, IL-6, and IL-8 and decreased excretion of Tamm-Horsfall glycoprotein in urine of patients with active lupus nephritis. 1086 35

Recent progress in biomarkers represents a paradigm shift in acute kidney injury (AKI) research. Most studies have evaluated the use of these biomarkers for early diagnosis of AKI. However, the role of novel biomarkers in predicting renal recovery, though less understood, holds great clinical promise. Accurate prediction would help physicians distinguish patients with poor renal prognosis in whom further therapy is unlikely to be useful from those who are likely to have good renal prognosis. Unfortunately, current general clinical severity scores (APACHE, SOFA, etc.) and AKI-specific severity scores are not good predictors of renal recovery. The biology of renal recovery requires the repopulation by surviving renal tubular epithelial cells with the assistance of certain renal epithelial cell and specific growth factors such as neutrophil gelatinase-associated lipocalin (NGAL), hepatocyte growth factor (HGF), epidermal growth factor, and insulin-like growth factor-1 (IGF-1), etc. These markers play a major role in the recovery process. This review will describe the mechanisms of the renal recovery, epidemiology, the role of conventional clinical predictors and finally the role of novel biomarkers (NGAL, HGF, IL-8, IL-18, TNFR-1, IGF-binding protein-7 and tissue inhibitor of metalloproteinase-2) in predicting renal recovery.
Nephron Clin Pract 2014
PMID:Repair or progression after AKI: a role for biomarkers? 2534 47