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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of Escherichia coli lipopolysaccharide (LPS) on adenylate cyclase have been tested using renal tubular membranes and renal glomeruli isolated from rats. E. Coli LPS did not stimulate glomerular and tubular basal adenylate cyclase activity whereas it was an activator in the presence of fluoride. The effect of E. Coli LPS was immediate but was greater after 20 min preincubation. Maximum stimulation of both glomerular and tubular fluoride sensitive adenylate cyclase occurred at 125 microgram/ml of E. Coli LPS with an apparent Km (dose corresponding to 50% of maximum stimulation) of 30 microgram/ml. Above 125 microgram/ml there was a decrease in adenylate cyclase activity. E. Coli LPS produced an increase in the maximum velocity of both enzymes but did not affect their affinity for adenosine triphosphate. E. Coli LPS did not potentiate the effect of parathyroid hormone on glomerular and tubular adenylate cyclase. The lipid A moiety which is common to all LPS whatever the original strain gave results similar to those obtained with the entire LPS. This effect was specific and did not depend on the phospholipidic structure in general since no activation was obtained in the presence of phosphatidylserine.
Nephron 1977
PMID:Effects of Escherichia coli lipopolysaccharide on renal glomerular and tubular adenylate cyclase. 33 75

Interleukin 6 (IL-6) is an autocrine growth factor of cultured mesangial cells (MC) and intraglomerular IL-6 production is suggested to be closely associated with the pathogenesis of human mesangial proliferative glomerulonephritis (mesPGN). In this study, to elucidate the mechanisms regulating the intraglomerular production of IL-6, we examined what kinds of stimuli are significant in the induction of IL-6 synthesis in vitro and in vivo. Incubation of cultured mesangial cells with interleukin 1 (IL-1) or bacterial lipopolysaccharide (LPS) induced significant IL-6 production, and intravenous injection of IL-1 or LPS into normal BALB/c mice induced significant intraglomerular IL-6 mRNA expression. Furthermore, we indicated in this study that IL-6 mRNA expression was augmented in the glomeruli of mice with immune complex-mediated glomerulonephritis.
Nephron 1992
PMID:Induction of interleukin 6 synthesis in mouse glomeruli and cultured mesangial cells. 143 93

CD23 is a surface marker of activated B cells as well as a low-affinity Fc receptor for IgE. In this study, we enumerated CD23-positive peripheral blood lymphocytes and evaluated their clinical significance in patients with IgA nephropathy (IgAN). Twenty-five patients with IgAN and 16 patients with non-IgA proliferative glomerulonephritis (PGN) were studied. Twenty-seven healthy adults served as controls. CD23-bearing cells were enumerated by flow cytometry, and serum IgE levels were measured by latex photometric immunoassay. Significant increases in the number of CD23-positive cells were observed in patients with IgAN (p less than 0.01) and PGN (p less than 0.05) compared with controls. A significant elevation of serum IgE levels was also observed in the patients with IgAN and PGN (p less than 0.05). No positive correlation between the number of CD23-positive cells and serum IgE levels was observed. We also examined the induction of surface CD23 expression on peripheral lymphocytes by interleukin (IL)-2, IL-3, IL-4, IL-5, IL-6, interferon (IFN)-gamma, IFN-alpha, phytohemagglutinin, concanavalin A, pokeweed mitogen, lipopolysaccharide and phorbol myristate acetate. IL-4 was revealed to have a significantly potent effect on the induction of cell surface CD23 compared with other stimulants. It was concluded that many patients with IgAN or PGN show high serum IgE levels and/or high CD23-positive cell counts in their peripheral blood, suggesting that hyperactivation of B cells might be involved in the development of IgAN and non-IgA PGN. It appeared that IL-4 may play a significant role in the etiology of these types of glomerulonephritis.
Nephron 1992
PMID:Increase of CD23-positive cells in peripheral blood from patients with IgA nephropathy and non-IgA proliferative glomerulonephritis. 153 1

The effect of peritoneal dialysate on the capacity of peripheral blood polymorphonuclear (PMNL) and mononuclear leukocytes (MNC) to release leukotriene B4 (LTB4) and tumor necrosis factor alpha (TNF alpha) was investigated in vitro. Following density gradient separation, aliquots of 5 x 10(6) PMNL or MNC were incubated in peritoneal dialysis fluid containing 1.5% glucose or Hanks' buffer (= control) for 1-2 h at 37 degrees C. TNF alpha and LTB4 production was stimulated with Escherichia coli lipopolysaccharide (LPS) and calcium ionophore A23187, respectively. MNC incubated in buffer and LPS produced (mean +/- SD) 1,006 +/- 522 pg TNF alpha/5 x 10(6) cells; no significant amounts of TNF alpha were detectable in the presence of dialysate. An inhibition of TNF alpha release was also observed in MNC exposed to bicarbonate-buffered dialysates (pH 7.40) and 4.25% and 1.5% glucose solution with physiologic osmolality. Incubation of PMNL in Hanks' buffer followed by A23187 stimulation led to production of 29.1 +/- 19.2 ng LTB4/5 x 10(6) cells, whereas glucose-incubated cells were refractory to ionophore stimulation (less than 0.1 ng LTB4/5 x 10(6) cells). The failure of dialysate-exposed leukocytes to release inflammatory mediators in response to adequate stimuli may contribute to the impairment of cellular host defense in the setting of continuous ambulatory peritoneal dialysis.
Nephron 1991
PMID:Leukotriene B4 and tumor necrosis factor release from leukocytes: effect of peritoneal dialysate. 165 27

A significant increase in gelatinolytic activity was observed in cultures of glomeruli from Heymann nephritic rats. Zymography of the culture medium indicated that the main gelatinase species has a molecular weight of 98 kilodaltons (kDa) and the characteristics of metalloproteinase. The 98-kDa gelatinase was detected in the culture medium of glomerular epithelial cells but not in those of endothelial and mesangial cells. Interleukin-1 beta, tumor necrosis factor-alpha and lipopolysaccharide dose-dependently increased gelatinase production by epithelial cells. These results suggest that the gelatinase secreted by cytokine-stimulated glomerular epithelial cells participates in the pathological process of Heymann nephritis.
Nephron 1990
PMID:Gelatinase secretion by glomerular epithelial cells. 196 1

We have investigated beta 2-microglobulin (beta 2M) synthesis and release by blood leukocytes and isolated mononuclear phagocytes. Recent interest in beta 2M has developed since the discovery that this protein forms amyloid fibrils in patients undergoing long-term, chronic hemodialysis and that these patients have greatly elevated levels of monomeric beta 2M in their circulation. Since hemodialysis-related factors that increase beta 2M production are unknown, we evaluated beta 2M production by freshly prepared leukocytes and monocyte-derived macrophages under a variety of conditions. We utilized a novel enzyme-linked immunoabsorbant assay to quantitate beta 2M concentrations, and monitored interleukin-1 and beta 2M synthesis by immunoprecipitation. Incubation of leukocytes with Cuprophan or Hemophan does not increase beta 2M release. Adherence of macrophages onto polystyrene or Cuprophan membranes induces neither interleukin-1 nor beta 2M synthesis or release. In contrast, interaction of macrophages with lipopolysaccharide, gamma-interferon, tumor necrosis factor, or interleukin-1 induces synthesis and release of beta 2 M, indicating that beta 2 M synthesis is increased during macrophage activation. Exposing leukocytes or macrophages to changes in osmotic or oncotic pressure induces a rapid release of beta 2M and interleukin-1 into the cellular medium. These results suggest that during hemodialysis, beta 2M production is more likely to result from endotoxin contamination, or osmotic and oncotic changes, rather than direct interaction of mononuclear phagocytes with Cuprophan membranes.
Nephron 1989
PMID:Hemodialysis-related induction of beta-2-microglobulin and interleukin-1 synthesis and release by mononuclear phagocytes. 250 49

The capacity of peripheral blood mononuclear cells (PBMC) to undergo spontaneous and induced interleukin-1 (IL-1) production was examined in 10 healthy controls and in 10 patients undergoing intermittent hemodialysis (HD) using cuprophane membranes. Extracellular and cytoplasmic IL-1 activity was assayed by biologic and radioimmunologic methods. Spontaneous extracellular IL-1 activity was low in the patient and the control groups. However, spontaneous cytoplasmic IL-1 activity was greatly increased in the patients. Both assays gave comparable results. In contrast, the IL-1 response to lipopolysaccharide was significantly decreased in PBMC from the patients compared to controls. From these results we conclude that PBMC from HD patients show functional signs of activation, but an impaired response to exogenous stimuli, such as endotoxin.
Nephron 1988
PMID:Altered interleukin-1 production in patients undergoing hemodialysis. 326 10

The influence of blood-membrane interaction on human peripheral blood monocyte tumor necrosis factor-alpha (TNF), interleukin-6 (IL-6), and interleukin-8 (IL-8) secretion was measured during hemodialysis of end-stage renal disease patients by in vitro stimulation of whole blood with lipopolysaccharide. Monocyte TNF and IL-6 secretion in vitro was reduced 30 min after start of dialysis session. In contrast, cellular IL-8 secretion did not change during hemodialysis. Comparison of the results of three different membranes indicates that the bioincompatibility of the dialysis membrane was reflected in both leukocytopenia and reduction of cellular TNF secretion. During treatment of normal whole blood in an ex vivo dialysis closed-loop circuit, the ability of monocytes to release TNF, IL-6, and IL-8 in vitro remained constant. This indicates that the reduced IL-6 and TNF secretion during standard hemodialysis was not due to a direct effect of contact between dialysis membranes and monocytes, but rather was a result of redistribution within the patients' leukocyte pool.
Nephron 1994
PMID:Effect of hemodialysis on peripheral blood monocyte tumor necrosis factor-alpha, interleukin-6, and interleukin-8 secretion in vitro. 801 41

The effect of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] deficiency, as well as of replacement therapy with 1 alpha-hydroxyvitamin D3[1 alpha-(OH)D3], on the production of tumor necrosis factor-alpha (TNF-alpha) by peripheral blood mononuclear cells (PBMC) and on the serum levels of soluble TNF receptors (sTNFRs) in hemodialysis (HD) patients was investigated. PBMC from HD patients without prior therapy with hydroxylated vitamin D3 analogs and from normal controls produced similar amounts of TNF-alpha, either spontaneously or after stimulation with lipopolysaccharide (LPS). After oral administration of 1 alpha-(OH)D3, a precursor of 1,25-(OH)2D3, LPS-induced TNF-alpha production by PBMC of HD patients was significantly higher than that of HD patients prior to the treatment or of healthy controls. Such treatment did not, however, affect spontaneous TNF-alpha production by PBMC. Serum concentrations of both soluble TNF receptors [sTNFR-A(p75) and sTNFR-B(p55)] were significantly higher in HD patients than in controls. The ratio of sTNFR-A/sTNFR-B decreased significantly in HD patients following 1 alpha-(OH)D3 therapy. These results suggest that therapy with 1 alpha-hydroxylated vitamin D3 analogs normally given to HD patients for the management of renal osteodystrophy may also regulate the in vivo activity of TNF-alpha.
Nephron 1994
PMID:Effect of 1 alpha-hydroxyvitamin D3 treatment on production of tumor necrosis factor-alpha by peripheral blood mononuclear cells and on serum concentrations of soluble tumor necrosis factor receptors in hemodialysis patients. 819 Jan 77

A study was conducted to determine whether intraperitoneal and oral administration of formalin-fixed gram-negative bacteria induced immunohistologically and ultrastructurally evident glomerular deposition of IgA and C3 in C3H/HeN mice. Separate treatments with strains of Pseudomonas aeruginosa, Escherichia coli, Haemophilus influenzae, Klebsiella pneumoniae, and two kinds of lipopolysaccharide (LPS) were used. Two mice in each treatment group were sacrificed at 10, 20 and 30 weeks of age to examine sequential glomerular changes. In addition to the intraperitoneal administration (IP) groups receiving whole formalin-fixed bacterial cells, cell precipitate and supernatant fractions of each bacterial strain after sonication were injected intraperitoneally once a week, and the mice were sacrificed at 30 weeks of age. Sequential quantitation or IgG, IgA or IgM in serum and the isotypes specific for each of the bacterial strains or LPS administered was performed by ELISA. The incidence of immunofluorescence positivity for glomerular IgA and C3 was 37-71 and 37-66.7%, respectively, in the IP groups that had received bacterial cells of each strain, which was significantly higher than that in the IP groups given LPS or in the controls. These results suggest that cell wall components common among gram-negative bacteria, other than LPS, play a major role in the glomerular deposition of IgA and C3. This is the first use of gram-negative bacteria to establish an active model of IgA nephropathy.
Nephron 1993
PMID:Experimental immunoglobulin A nephropathy induced by gram-negative bacteria. 824 80


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