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

Purified lipopolysaccharide (LPS) from Pseudomonas aeruginosa was used as an antigen for immune complex (IC) formation in vitro together with hyperimmune sera from chronically P. aeruginosa-infected patients with cystic fibrosis (CF). P. aeruginosa LPS by itself did not induce an oxidative burst in human neutrophil granulocytes (PMN)s measured by chemiluminescence (CL). This was also the case using hyperimmune CF serum alone. In contrast, P. aeruginosa LPS together with CF serum did induce a CL response. The CL responses varied depending on the sera used for IC formation, and were reduced when protein A preabsorbed sera were used. PEG precipitation of the ICs from the mixture increased the CL response. These findings indicate that the CL responses induced by the mixture of P. aeruginosa LPS and CF serum were due to IC formation and an Fc-mediated stimulation of the PMNs. It is concluded that ICs made from sera of chronically infected CF patients and purified P. aeruginosa LPS are biologically active in terms of activating PMNs, and may contribute to the lung tissue damage seen in this group of patients.
 ...
PMID:Induction of oxidative burst response in human neutrophils by immune complexes made in vitro of lipopolysaccharide and hyperimmune serum from chronically infected patients. 828 97

We studied the effects of systemic endotoxemia on small intestinal absorption in an in vivo animal model. Seven adolescent Yorkshire swine underwent creation of 25 cm distal ileal Thiry-Vella fistulae. After 1 week recovery, the fistulae were perfused with a solution of glucose and electrolytes labeled with 14C-PEG, and net absorption of water, Na+, Cl-, and glucose was calculated. Animals were studied under three different conditions: (1) Basal fasting state, (2) immediately after intravenous injection of E. coli lipopolysaccharide (LPS; 250 micrograms/kg), and (3) 24 hours after LPS. Water, Na+, and Cl- absorption was significantly reduced 2 hours after LPS, but recovered to baseline values by the third hour after LPS. Twenty-four hours after LPS water, Na+, and Cl- absorption was significantly decreased below baseline values. Glucose absorption after LPS paralleled that of water and electrolytes, except that the transient early recovery was not observed. Histological studies of the ileum after LPS showed marked epithelial inflammation at 6 hours, villous atrophy at 24 hours, and signs of recovery at 7 days. Intestinal absorption of water, electrolytes, and glucose is adversely affected in the immediate and early periods after an endotoxemic episode, but the histological epithelial injury secondary to endotoxemia is reversible.
 ...
PMID:Small intestinal absorption during endotoxemia in swine. 881 57

Endotoxin [lipopolysaccharide (LPS)] is a cell wall polymer derived from Gram-negative bacteria that stimulates macrophages to produce a variety of inflammatory mediators. In these studies, we examined LPS-stimulated formation of tumor necrosis factor-alpha (TNF-alpha) by cultured rat Kupffer cells. Cytochalasin B and methylpalmitate, blockers of endocytosis, decreased LPS-stimulated TNF-alpha release by > 92%. Bafilomycin A, monensin, and chloroquine, which prevent endosomal acidification, also blocked LPS-stimulated release of TNF-alpha by > 90%. Cytochalasin B and bafilomycin A decreased TNF-alpha mRNA levels by > 90% after LPS stimulation. Consistent with the requirement for LPS uptake and processing was the observation that Kupffer cells required 30 min of contact with LPS for maximal TNF-alpha release. LPS-stimulated TNF-alpha release was unaltered by incubation in Ca(2+)-free ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid medium, and A-23187, a Ca2+ ionophore, failed to stimulate TNF-alpha release in the absence of LPS. However, nisoldipine, a Ca2+ channel blocker, suppressed LPS-stimulated TNF-alpha release in cells cultured both in Ca(2+)-containing and Ca(2+)-free media. Although thapsigargin did not block TNF-alpha release, this depleter of intracellular Ca2+ stores blocked LPS-stimulated TNF-alpha synthesis in Ca(2+)-free medium and decreased TNF-alpha mRNA levels by 80%. Furthermore, LPS induced a late rise in intracellular free Ca2+ demonstrated by video microscopy of fura 2-loaded Kupffer cells. De novo protein and RNA synthesis were required, since cycloheximide and actinomycin D also inhibited LPS-stimulated TNF-alpha release. We compared free TNF-alpha secreted into culture supernatants with cell-associated TNF-alpha and found that cytochalasin B, bafilomycin A, chloroquine, monensin, and nisoldipine did not increase bound, cell-associated TNF-alpha. We conclude that endocytosis and endocytic processing may be necessary for LPS-stimulated TNF-alpha release from Kupffer cells. Ca2+ release, regulated by dihydropyridine-sensitive Ca2+ channels, also appears to be necessary for LPS-induced signaling and may arise from intracellular stores associated with the endosome/lysosome compartment.
 ...
PMID:Endocytosis and Ca2+ are required for endotoxin-stimulated TNF-alpha release by rat Kupffer cells. 894 8

The proinflammatory cytokine, interleukin-1 (IL-1) is elevated in the Alzheimer's disease (AD) brain. Studies from our laboratory have demonstrated that beta-amyloid (A beta) 1-42, fibrillar A beta 1-40 and A beta 25-35 induce the release of IL-1 beta from activated THP-1 cells, a human monocyte cell line. A beta also is chemotactic for primary rodent microglia and peritoneal macrophages. We hypothesize that A beta is a chemokine and induces these responses by interaction with chemotactic receptors. If this is true, then these A beta-induced responses should be calcium-dependent and require activation of pertussis toxin-sensitive G-proteins. To test this hypothesis, THP-1 cells were grown in culture with lipopolysaccharide (LPS) and incubated with A beta 1-42 (5 muM) in the presence and absence of a calcium chelator, an inhibitor of intracellular calcium mobilization, a calcium channel blocker, or pertussis toxin, a bacterial endotoxin which uncouples G proteins from receptors by catalyzing the ADP ribosylation of cysteine near the carboxy-terminus of the alpha subunit. The media was collected and IL-1 beta present in the media was measured using an ELISA. Treatment of LPS-activated THP-1 cells with A beta 1-42 significantly elevated IL-1 beta released into the media as previously shown. Addition or ethylene glycol-bis (beta-aminothyl ether) N,N,N'N'-tetraacetic acid (EGTA) (0.5 mM), a calcium chelator, to the media blocked A beta-induced IL-1 beta release, but had no effect on LPS-activated THP-1 cell release of IL-1 beta. The presence of 3,4,5-trimethoxybenzoic acid 8-(diethyl amino)-octyl ester (TMB-8), an inhibitor of intracellular calcium mobilization, as well as nickel chloride, a non-specific calcium channel blocker, in the media also inhibited A beta-induced IL-1 release from LPS-activated THP-1 cells. IL- 1 beta release from activated THP-1 monocytes incubated with TMB-8 and nickel chloride without A beta remained at baseline values. Pretreatment of THP-1 monocytes with pertussis toxin for 4 h, followed by LPS activation and incubation with A beta, antagonized the release of IL-1 beta from these cells, but did not alter IL-1 beta release from activated THP-1 monocytes. These data suggest that A beta-induced IL-1 beta release from these cells is calcium-dependent and requires the activation of specific G-proteins. These findings are consistent with known second messengers that are activated following stimulation of chemotactic receptors.
 ...
PMID:beta-Amyloid-induced IL-1 beta release from an activated human monocyte cell line is calcium- and G-protein-dependent. 914 72

Diarrhea is a common manifestation of sepsis. We hypothesized that endotoxin may impair colonic absorption of water and electrolytes, an effect which may be related to altered liquid transit in the colon. Five dogs underwent construction of 50-cm colonic Thiry-Vella fistulas (TVF). Following recovery, absorption studies were performed by perfusing the TVF with an isotonic solution at 2.9 ml/min containing polyethylene glycol (5 g/L). Fasting and postprandial colonic absorption of water, electrolytes, and glucose were determined. Liquid transit was assessed by bolus of a nonabsorbable marker (PSP) instilled into the proximal end of the TVF. Following completion of the baseline studies, each dog was given a single dose of Escherichia coli lipopolysaccharide 200 micrograms/kg i.v. and the studies were repeated daily for the next 3 days. Following endotoxin bolus, colonic absorption of water and sodium were decreased during fasting, while postprandial colonic absorption of water was also decreased. Colonic absorption of water and sodium returned to baseline values on postendotoxin day 2. Colonic secretion of potassium was decreased on postendotoxin days 1 and 3 in both the fasting and the fed periods. Fasting and postprandial liquid transit was also rapid on postendotoxin day 1, which correlated with the decreased absorption seen on that day. Liquid transit returned to baseline values on postendotoxin day 2. We conclude that endotoxin temporarily impairs postprandial colonic absorption, which may be due to the rapid liquid transit that occurs. These effects may contribute to the diarrhea seen during and after septic episodes.
 ...
PMID:Endotoxin temporarily impairs canine colonic absorption of water and sodium. 953 70

Our previous studies have shown that the degree of damage to a liposome corresponds to the variability of the animal species from which the serum comes, and that a complement activating factor (CAF) plays an important role in inducing the activation of the complement system, ultimately leading to the lysis of the liposomes. In this study, our attention focused on the characterization of the bovine serum factor (bCAF) that is involved in complement-mediated immune lysis of the liposome. The active fraction containing CAF partially purified with PEG and ammonium sulfate results in marked activation of the complement system via the alternative pathway when interacted with CAF-depleted serum, whereas the active fraction or CAF-depleted serum alone does not activate the complement. The interaction between lipopolysaccharide (LPS), heparin, zymosan or their mixture in place of CAF and CAF-depleted serum does not result in any significant activation of the complement system. Results from pretreatment with rabbit anti-bovine IgM IgG and rabbit anti-bovine IgG IgG indicate that activation of the complement system is not attributable to the antibody which is generally involved in activation of complement via the classical pathway. The results have further been proven by pretreatment with Concanavalin A (Con A) sepharose and protein G sepharose ruling out the possibility of antibody-mediated activation of complement. Our studies on collagenase and trypsin digestion demonstrate that the relative activity of CAF does not diminish with increase in collagenase concentration, and decreases with increase in trypsin concentration, strongly indicating that CAF does not have a collagen-like domain in its structure. The relative activity of CAF is dramatically inhibited after reduction with 2-mercaptoethanol (2-ME), clearly demonstrating that CAF is sensitive to reduction with 2-ME and confirming a sulhydryl-dependent protein. The optimal activity of CAF is observed in the range of 35-45 degrees C and its half-life at 37 degrees C is about 105 h. Furthermore, the relative activity of CAF increases and gradually approaches a plateau level with the increase of Mg2+ concentration. Obviously, complement activation induced by CAF depends on adequate Mg2+ concentration, confirming that this dependence is characteristic of the alternative pathway.
 ...
PMID:Characterization of bovine serum factor triggering the lysis of liposomes via complement activation. 958 79

To evaluate the biocompatibility of dialysis membranes, blood samples were collected from 10 hemodialysis patients immediately before dialysis and peripheral blood mononuclear cells were isolated. The 3.0 x 10(5) cells/ml were then passed 30 times through modules made of a polyethylene glycol-grafted cellulose membrane, a polyacrylonitrile membrane, and a polysulfone membrane. Expression of messenger RNA for tumor necrosi factor-alpha (TNF-alpha) was determined. Cells were also cultured for 2 h with and without lipopolysaccharide and TNF-alpha levels in the supernatant were measured. TNF-alpha messenger RNA expression was significantly higher immediately after passage through the polyacrylonitrile membrane compared with the other membranes. Cells cultured without lipopolysaccharide, produced significantly less TNF-alpha after passage through the polysulfone membrane, while lipopolysaccharide significantly increased TNF-alpha production by cells passed through the polyacrylonitrile membrane. These results suggest that biocompatibility differs even among dialysis membranes believed to cause no complement activation.
 ...
PMID:Effects of dialysis membranes on the kinetics of tumor necrosis factor-alpha production by peripheral mononuclear cells in chronic hemodialysis patients. 974 92

Enteral feeding during and after episodes of sepsis may be beneficial. The aim of our study was to determine the effects of a single sublethal dose of endotoxin on canine jejunal absorption. Following a 240 kcal liquid meal, absorption studies were performed in eight dogs with 75 cm jejunal Thiry-Vella fistulas. These fistulas were perfused with an isotonic solution containing polyethylene glycol to calculate absorption. Each dog was then given a single dose of Escherichia coli lipopolysaccharide, 200 microg/kg intravenously, and the studies were repeated for the next 3 days. Following endotoxin bolus infusion, net absorption of water, electrolytes, and glucose was decreased for 2 days and returned to baseline values on postendotoxin day 3. A single sublethal dose of endotoxin temporarily impairs canine jejunal absorption. Although enteral feeding may be advantageous, jejunal absorption may be temporarily impaired following an episode of endotoxemia.
 ...
PMID:Endotoxin temporarily impairs canine jejunal absorption of water, electrolytes, and glucose. 983 60

Our previous study has shown that the rapid and sufficient activation of complement by Salmonella lipopolysaccharide occurs in genetically resistant (Ityr) A/J mice. To assess whether the level of complement activation by a virulent strain of Salmonella typhimurium regulates the level of murine natural resistance, we compared levels of serum complement activation by S. typhimurium and kinetics of serum-opsonized S. typhimurium grown in macrophages using several strains of resistant (Ityr) and susceptible (Itys) mice. Itys macrophages killed intracellular S. typhimurium to the same extent as did Ityr macrophages when the pathogen was opsonized with Ityr serum. Opsonization of S. typhimurium with Itys serum reduced intracellular killing activity in Ityr macrophages to the same level as seen with Itys macrophages. Incubation of S. typhimurium with 25% Mg2+ EGTA (5 mm MgCl2-3 mm ethylene glycol-bis (beta-aminotheyl either)-N,N,N',N'-tetraacetic acid)-chelated Ityr serum resulted in higher levels of C3 deposition onto the surface of this bacteria, C3b generation and also C3 consumption, compared with that with Mg2+ EGTA-chelated Itys serum. Opsonization of S. typhimurium with A/J serum prior to infection increased early resistance in Itys mice. Infection with a virulent strain of S. typhimurium induced the expression of interleukin-10 (IL-10) mRNA at higher levels in C57BL/6 mice than in A/J mice. However, opsonization of S. typhimurium with A/J serum decreased bacterial growth in the spleen of C57BL/6 mice to the same level as observed for A/J mice in association with decreased expression levels of IL-10 mRNA. Moreover, administration of anti-C3 antibodies reduced the resistance of A/J mice in association with a decrease in serum levels of C3. These results indicate that the high level of complement activation via the alternative pathway in Ityr serum by a virulent strain of S. typhimurium reduces the virulence of this pathogen, which may contribute to the full expression of Ity phenotype in Ityr mice.
 ...
PMID:The full expression of the ity phenotype in ityr mice requires C3 activation by Salmonella lipopolysaccharide. 989 57

The role of calcium in transducing the signal for interleukin-1 (IL-1) secretion was examined in the MQ-NCSU chicken macrophage cell line. Cells were maintained in RPMI 1640 medium supplemented with 5% chicken serum and antibiotic-antimycotic solution at 40 C and 5% CO2. The effects of stimulation with lipopolysaccharide (LPS), calcium ionophore A23187, or a combination of both on IL-1 secretion were examined. Calcium ionophore A23187 did not replace LPS in MQ-NCSU stimulation but the LPS + A23187 combination stimulated more IL-1 than ionophore alone in these cells. The combination of LPS and ionophore did not increase IL-1 secretion above the levels observed with LPS alone. No synergistic effects between LPS and A23187 were evident. In order to demonstrate that IL-1 secretion by the MQ-NCSU cells is a calcium-dependent process, ethylene glycol bis(beta-aminoethyl ether)N,N,N',N'-tetraacetic acid (EGTA) was used to chelate free calcium in the cultures. Incorporation of 5 mM EGTA in the cultures lowered IL-1 stimulated by LPS + A23187 to control levels. Addition of 5 mM CaC12 to EGTA-suppressed cultures restored IL-1 secretion. These results indicate that the calcium ionophore, A23187, augments IL-1 secretion by LPS-stimulated MQ-NCSU macrophages and that IL-1 secretion by these cells is a calcium-dependent process.
 ...
PMID:Calcium dependency of interleukin-1 secretion by a chicken macrophage cell line. 1002 50


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>