Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Increase of CD23-positive cells in peripheral blood from patients with IgA nephropathy and non-IgA proliferative glomerulonephritis. 153 1

Peripheral blood B-lymphocyte markers and functions were observed in 21 patients with IgA nephropathy (IgA NP) and in 16 controls. IgA NP B lymphocytes expressed significantly higher positivity with Leu 1 (CD 5) monoclonal antibody than controls. CD 5 positive B lymphocytes are thought to be a distinct subset of the B cells (autoregulatory B lymphocytes) inducible in IgA NP by lipopolysaccharide (LPS) stimulation parallel to the higher expression of surface IgM heavy chain positivity. The activated state of IgA NP B lymphocytes has been proved by their higher OKIa (HLA-DR) positivities but lower IOB1a (CD 21, C3d-receptor) and decreased IgG-Fc-receptor (ox-rosette) expression. IgA NP B lymphocytes showed a higher IgA but also IgG and IgM polyclonal immunoglobulin production than control B lymphocytes in co-cultures with T lymphocytes. Not only regulatory T lymphocyte subsets but also serum derived from IgA NP patients stimulated the immunoglobulin production of IgA NP B cells.
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PMID:Peripheral B-lymphocyte markers and function in IgA nephropathy. 210 34

Peripheral blood B-lymphocyte markers and functions were observed in 21 patients with IgA nephropathy (IgA NP), 18 patients with systemic lupus erythematosus (SLE) and 16 controls. IgA NP B-lymphocytes similarly to that of SLE B-lymphocytes expressed significantly higher positivity with Leu 1 (CD 5) monoclonal antibody than controls. CD 5 positive B-lymphocytes are thought to be a distinct subset of the B-cells (autoregulatory B-lymphocytes) inducible in IgA NP by lipopolysaccharide (LPS) stimulation in parallel to their expression of surface IgM heavy chain positivity. The activated state of IgA NP B-lymphocytes have been proved by their higher OKIa (HLA-DR) positivities but lower IOB1a (CD 21, C3b-receptor) and decreased IgG-Fc-receptor (ox- rosette) expression. IgA NP B-lymphocytes showed a higher IgA but also IgG and IgM polyclonal immunoglobulin production than control B-lymphocytes in co-cultures with T-lymphocytes. Not only regulatory T-lymphocyte subsets but also serum derived from IgA NP patients stimulated the immunoglobulin production of IgA NP B-lymphocytes.
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PMID:[Markers of peripheral B lymphocytes and their function in IgA nephropathy]. 220 18

Prolonged dietary exposure of mice to the trichothecene vomitoxin induces abnormally high levels of serum IgA and kidney mesangial IgA accumulation in a manner that is highly analogous to the human glomerulonephritis IgA nephropathy. In this study, the capacity of Peyer's patch and splenic lymphocytes to produce IgA and IgG were compared in B6C3F1 mice that were fed diets with and without 25 ppm vomitoxin for up to 12 wk. Serum IgA increased 2-, 4- and 8-fold after 4, 8 and 12 wk, respectively, of vomitoxin exposure and it became the primary serum isotype, whereas serum IgG was unaffected. On termination of the experiment there were increased numbers of IgA-secreting cells in Peyer's patches after 8 wk of toxin exposure and in the spleen after 4, 8 and 12 wk of toxin exposure. There were also increased numbers of IgG-secreting cells in Peyer's patches on termination of the experiment at 4, 8 and 12 wk but no effects was observed in the spleen. Supernatant IgA and IgA-secreting cell numbers were also markedly elevated in lymphocyte cultures obtained from Peyer's patches and, to a lesser extent, from spleens of treated mice compared with controls. Based on output of treated mice relative to corresponding controls, IgA secretion was greatest in concanavalin-A-stimulated and unstimulated Peyer's patch cultures. Enhanced IgG secretion and IgG-secreting cells were also observed in mitogen-stimulated and unstimulated Peyer's patch lymphocyte cultures of treated relative to control mice, but differences in splenocyte cultures were negligible. Based on total Ig output, IgA production was 8- to 20-fold greater than IgG production in both control and treatment Peyer's patch cultures. In contrast, vomitoxin treatment caused a shift from primarily IgG production in lipopolysaccharide-stimulated spleen cultures to equivalent IgA production. These data provide in vitro evidence that ingestion of vomitoxin promotes terminal differentiation of IgA-secreting progenitors in the Peyer's patch and, to a lesser extent, in the spleen. These functional changes are consistent with the shift from IgG to IgA as the primary serum isotype.
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PMID:Effect of dietary administration of the trichothecene vomitoxin (deoxynivalenol) on IgA and IgG secretion by Peyer's patch and splenic lymphocytes. 227 98

In order to further characterize monocyte function in patients with lipoid nephrosis (LN), we studied the production of interleukin-1 (IL-1). In this study we examined the ability of peripheral blood monocytes (PBM) from LN patients to produce this monokine in vitro under the stimulus of bacterial lipopolysaccharide (LPS). The levels of IL-1 were decreased in patients with LN compared with those in normal controls and lower in LN patients with nephrotic syndrome (NS) than in those without NS. In contrast, the values in IgA nephropathy (IgAN) patients with or without NS did not differ from normal subjects. The addition of indomethacin, an inhibitor of prostaglandin synthesis, partially restored this defect. These results suggest that the impaired IL-1 production of LN PBM is probably attributable, at least in part, to increased prostaglandin production and possibly influences the immune status of LN patients.
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PMID:Decreased production of interleukin-1 by monocytes from patients with lipoid nephrosis. 278 18

IL-8 is a chemotactic cytokine with proinflammatory and growth-promoting activities. The release of IL-8 was measured in supernatants of cultured peripheral blood monocytes (PBM) that were obtained from patients with glomerulonephritis (GN) and healthy controls. Spontaneous and lipopolysaccharide (LPS)-induced IL-8 release was significantly higher in PBM isolated from patients with IgA nephropathy (IgAN) and membranous nephropathy (MN) compared with normal controls. These results raise the question of whether IL-8 contributes to the ongoing pathogenesis of GN. We cannot relate IL-8 release to clinical and laboratory parameters in IgAN and MN patients. Thus, disease progression in vivo may not be accompanied by increased or sustained IL-8 release.
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PMID:IL-8 release from cultured peripheral blood monocytes of patients with glomerulonephritis. 781 1

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.
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PMID:Experimental immunoglobulin A nephropathy induced by gram-negative bacteria. 824 80

The release of tumor necrosis factor-alpha (TNF) was measured in supernatants of cultured peripheral blood monocytes (PBM) that were obtained from patients with glomerulonephritis (GN) and healthy controls. Spontaneous and lipopolysaccharide (LPS)-induced TNF release were significantly higher in PBM isolated from patients with IgA nephropathy (IgA N) and membranous nephropathy (MN) as compared to normal controls. These biological activities were neutralized by a specific antibody to TNF. In patients with IgA N and MN TNF levels did not correlate with clinical disease activity. We conclude that in vitro GN PBM are hyperactive in their release of TNF, and that this enhanced release of TNF in vitro may reflect a secondary consequence of monocyte activation rather than a primary cellular defect in GN.
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PMID:Increased release of tumor necrosis factor-alpha by monocytes from patients with glomerulonephritis. 840 69

IL-10, a cross-regulatory cytokine produced by several cell types, including monocytes, is known to stimulate B cell growth and maturation and to inhibit cytokine production. In order to characterize further monocyte function in patients with lipoid nephrosis (LN), the release of IL-10 was measured in supernatants of cultured peripheral blood monocytes (PBM) that were obtained from LN patients and healthy controls. Spontaneous and lipopolysaccharide (LPS)-induced IL-10 release was decreased in patients with LN compared with those in normal controls and lower in LN patients with the nephrotic syndrome (NS) than in those without NS. In contrast, the values in IgA nephropathy (IgAN) patients with or without NS did not differ from normal subjects. There was a negative correlation between IL-10 concentration and the quantity of vascular permeability factor (VPF) released in LN patients. These imply that there is a relative deficit in IL-10 release in active LN, which suggests the possibility that inadequate release of IL-10 may lead to increased VPF activity in active LN patients and the measurements of IL-10 may be of value for monitoring kidney disease. The data provide the first detailed analysis of IL-10 in a group of patients with LN.
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PMID:Decreased release of IL-10 by monocytes from patients with lipoid nephrosis. 853 79

The effect of recombinant human interleukin-10 (IL-10) on the in vitro cytokine secretion of peripheral blood monocytes (PBM) was evaluated in patients with IgA nephropathy (IgAN). Significantly increased spontaneous and lipopolysaccharide (LPS)-stimulated secretion of tumor necrosis factor-alpha and interleukin-8 was determined in PBM cultures of IgAN patients compared to those of normal controls. In the present study IL-10 inhibited the spontaneous as well as the LPS-stimulated cytokine secretion of PBM in IgAN. A significant inhibitory effect of IL-10 was observed in cultures of PBM from IgAN patients as well as from normal controls. When both LPS and anti-IL-10 antibody were added together to the PBM, a further increase in LPS-enhanced secretion of cytokines occurred. This study provides some novel information showing the inhibitory effects of IL-10 on cytokine secretion by PBM derived from IgAN patients.
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PMID:Spontaneous and lipopolysaccharide-stimulated secretion of cytokines by peripheral blood monocytes in IgA nephropathy is inhibited by interleukin-10. 877 61


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