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)

A large number of bacterial species are causative agents of respiratory tract disease. The discussion will center on three infections selected because they represent different problems in control on the basis of epidemiologic and immunochemical factors. Group A hemolytic streptococci are common upper respiratory tract pathogens which may initiate severe non-suppurative sequelae such as rheumatic fever and glomerulonephritis. Recent progress concerning M protein vaccines will be reviewed. Pneumococci are still the most frequent cause of pneumonia at all ages. Pneumococcal vaccines are the prototype for purified polysaccharide vaccines since their effectiveness was demonstrated 30 years ago. The major problem in vaccination is the very large number of capsular serotypes. Pseudomonas aeruginosa represents the relatively new problem of gram-negative bacterial infections in the immunodepressed host. Demonstration of seven immunotypes as the cause of 90% of human infections has led to preparation of a multivalent vaccine composed of lipopolysaccharide antigens. Current knowledge of this vaccine will be discussed.
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PMID:Problems and progress towards vaccination against bacterial infections of the respiratory tract. 23 8

Polyclonal activation of lymphocytes and immune complex-mediated glomerular lesions were induced in C57Bl/6 mice by injecting bacterial lipopolysaccharide (LPS) twice a week for 2 weeks. The usefulness of such a model for in vivo evaluation of immunomodulatory and therapeutic effects of drugs, was investigated by treating mice with DIAM4, a cyclophosphazenic compound known to modulate polyclonal activation of lymphocytes and to prevent mouse lupus nephritis. Prevention of LPS-triggered lymphocyte polyclonal activation and glomerular lesions was observed in the DIAM4-treated mice. Such a model can be used conveniently to select compounds effective in the treatment of immune glomerulonephritis.
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PMID:An in vivo model for the experimental selection of drugs able to prevent immune complex glomerulonephritis. 138 91

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.
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PMID:Induction of interleukin 6 synthesis in mouse glomeruli and cultured mesangial cells. 143 93

A crescentic glomerulonephritis (GN) model was induced by intravenous injection of rabbit anti-mouse glomerular basement membrane (GBM) antiserum and lipopolysaccharide (LPS) in BALB/c mice, heterozygous mice and nude mice respectively, in order to detect the T-cells effects on the development of crescentic GN. The immunofluorescence and morphological changes of glomeruli in different groups of animals were compared. Intense fluorescence (4+) of rabbit IgG could be found along the GBM in liner pattern in all the animals. Intense (3(+)-4+) mouse IgG was also found along the GBM in liner pattern in the normal and heterozygous mice, but could not be identified in the nude mice. The normal mice developed typical crescentic GN, characterized by serious degeneration and destruction of GBM, fibrin deposition and crescents formation, 3-6 weeks after the injection. The heterozygous mice only developed mild proliferation of the mesangial cells in the glomeruli but there was no glomerular lesion detected in the nude mice. It suggests that the glomerular immune damage requires the participation of functional T-cell.
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PMID:[The roles of T cells in experimental crescentic glomerulonephritis]. 149 70

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

Nitrite (NO2-) is the major end product of nitric oxide (NO) production in cell culture. The authors have examined nitrite production by glomeruli in in situ immune complex glomerulonephritis in the rat. Glomerulonephritis was induced by unilateral renal perfusion of cationized human gamma G immunoglobulin (IgG) in preimmunized rats. NO2- was measured in culture supernatants of isolated glomeruli after 48 hours. NO2- was produced by nephritic glomeruli with a maximum 4 days after induction of glomerulonephritis (24.4 +/- 11.4 pmol/glomerulus/48 hours). Production was increased by lipopolysaccharide (LPS; 1 micrograms/ml) (54 +/- 4.9 pmol/glomerulus; P less than 0.001). NO2- production was inhibited by the nitric oxide synthase inhibitor NG-monomethyl-L-arginine demonstrating synthesis through NO. Dexamethasone (10(-7) mol/l [molar]) reduced LPS-stimulated production by peritoneal macrophages and nephritic glomeruli (P less than 0.01). Macrophages isolated from nephritic glomeruli produced NO2- (4.9 +/- 0.6 nmols/10(5) cells). The production of NO by nephritic glomeruli has implications for mechanisms of glomerular injury and glomerular hemodynamics. The effect of dexamethasone may explain in part the ameliorative effect of steroids in glomerulonephritis.
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PMID:Glomerular nitrite synthesis in in situ immune complex glomerulonephritis in the rat. 195 26

A model of crescentic glomerulonephritis (GN) in mice was induced by intravenous injection of rabbit anti-mouse glomerular basement membrane (GBM) antiserum and lipopolysaccharide. The procedure was carried out in BALB/c mice, heterozygous mice and nude mice. In order to examine the role of T cells in the pathogenesis of crescentic GN, immunofluorescent and morphologic changes in the glomeruli of these animals were studied. Intense (4+) linear deposition of rabbit IgG was found along the GBM of all test animals. Intense (3(+)-4+) linear deposition of mouse IgG along the GBM was present in normal and heterozygous mice, but not in nude mice. Normal mice developed typical crescentic GN characterized by severe degeneration and destruction of GBM, fibrin deposition and crescent formation 3-6 weeks after injection. Heterozygous mice only developed mild mesangial proliferation. No glomerular lesions were seen in nude mice. These preliminary data suggest that glomerular immunologic damage requires the participation of functional T cells, and that the induction of typical crescentic GN requires integral T-cell function.
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PMID:Correlation between T cells and experimental crescentic glomerulonephritis. 212 53

Activated macrophages synthesize nitric oxide (NO) from L-arginine. In culture, the major stable end product is nitrite (NO2). Activated macrophages accumulate in glomeruli and are responsible for injury in experimental immune complex glomerulonephritis. We examined NO2- production by isolated glomeruli and urinary NO2- in accelerated nephrotoxic nephritis in the rat. Normal glomeruli did not produce NO2- spontaneously or when stimulated with lipopolysaccharide (LPS) (1 microgram/ml) or A23187 (2 microgram/ml). Cultured mesangial cells at first or seventh passage did not produce NO2- spontaneously or when stimulated. Nephritic glomeruli spontaneously produced NO2 at all times studied; this production was maximal at 24 hours after induction of glomerulonephritis (158.4 +/- 8.4 nmol/48 hr/ml, N = 3). The production of NO2- was inhibited 75 to 100% by NG-monomethyl-L-arginine (L-NMMA), and this inhibition was reversed by L-arginine, indicating NO2- production from L-arginine via NO. The production of NO2- was increased by LPS (1 microgram/ml) at 2, 7 and 21 days. NO2- was undetectable in normal rat urine; however, it was present in urine of rats with glomerulonephritis (Day 0 to 1:8161 +/- 2605 nmol/24 hr. N = 12). The production of NO in nephritic glomeruli may have implications for both the mechanism of glomerular injury and glomerular hemodynamics.
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PMID:Glomeruli synthesize nitrite in experimental nephrotoxic nephritis. 215 84

Systemic lupus erythematosus is a multifactorial systemic disease in which genetic, immunologic, hormonal, and environmental factors may contribute to disease pathogenesis. Bacterial products (eg, bacterial lipopolysaccharide [LPS]) induce a lupuslike disease in normal mice and trigger an early and accelerated form of lupus nephritis in NZB/W mice. To investigate whether the mechanism by which LPS accelerates nephritis in the NZB/W mice involves interference with processing of immune complexes (IC), we administered LPS to NZB/W mice for 5 weeks and probed the kinetics of removal, liver uptake, and organ localization of a subsaturating dose of radiolabeled IC (2.5 mg of bovine serum albumin-antibovine serum albumin). Control NZB/W mice received vehicle (saline) alone. In NZB/W exposed to LPS, features of polyclonal B-cell activation (PBA) were enhanced, anti-DNA antibodies were raised, and a proliferative glomerulonephritis developed that was associated with renal insufficiency and substantial proteinuria. This LPS-accelerated nephritis could not be attributed to altered complement concentration, to altered blood cell carrier function, to delayed removal of pathogenic (large-sized) ICs from the circulation, to impaired liver uptake of ICs, or to enhanced localization of ICs in kidney. The findings indicate that transformation of nephritis is probably the result of LPS-induced PBA, that defective processing of pathogenic IC is not a contributory factor to nephritis, and that mechanisms other than passive renal localization of circulating ICs must be operative.
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PMID:Bacterial lipopolysaccharide transforms mesangial into proliferative lupus nephritis without interfering with processing of pathogenic immune complexes in NZB/W mice. 222 Oct 21

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


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