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At least 1,333 records · Page 74Linked to original sources
PubMed1994

Structure of the unusual trisaccharide lipopolysaccharide component produced by a symbiotically defective mutant of Rhizobium leguminosarum biovar viciae.

The structure of an unusual trisaccharide component isolated from the lipopolysaccharide (LPS) of a Tn5 mutant of Rhizobium leguminosarum biovar viciae VF39 which is defective in infection of its host plant has been elucidated. This mutant also appears to be defective in the synthesis of a tetrasaccharide component normally synthesized by the wild-type organism. The three glycosyl components are galactose, mannose, and 3-deoxy-D-manno-2-octulosonic acid (Kdo). Mannose is linked to the 5-position and galactose to the 7-position of the 3-deoxy-2-octulosonic acid residue (Kdo). Both hexosyl components are in the alpha-pyranosyl form. In the isolated molecule the octulosonic acid appears to be present as its gamma-lactone. However, in the lipopolysaccharide molecule, it is most likely present in the pyranosyl form. The structure was determined by 1H NMR spectroscopy and methylation analysis as well as by fast-atom-bombardment mass spectrometry of the peracetylated and per(trideuterio) acetylated oligosaccharides. Small amounts of the methylation analysis product of another tetrasaccharide different to normal tetrasaccharide component made by the wild-type organisms were detected. This indicates that in this mutant, there is a block in the synthesis of the normal tetrasaccharide component in addition to a switch in the synthesis of the LPS type.

Carbohydrate Conformation↗
PubMed1997

Structure of a new 6-deoxy-alpha-D-talan from Burkholderia (Pseudomonas) plantarii strain DSM 6535, which is different from the O-chain of the lipopolysaccharide.

An O-acetylated homopolysaccharide of 6-deoxy-D-talose (6-deoxy-alpha-D-talan polymer) was isolated from Burkholderia (Pseudomonas) plantarii strain DSM 6535 by extraction with 2-propanol. The structure (1) of the trisaccharide repeating unit of the polysaccharide was established by studies of the intact and O-deacetylated polysaccharides using methanolysis, methylation analysis, 1H and 13C NMR spectroscopy, including 2D COSY, heteronuclear 13C, 1H COSY, 1D NOE, and computer-assisted analysis of 1D 13C NMR spectra. The remaining material after extraction of the biomass with 2-propanol showed to be a lipopolysaccharide with an O-specific polysaccharide chain having a different structure (2), which has been found previously in lipopolysaccharides of a number of other Gram-negative bacteria. [formula: see text]

Antigens, Bacterial↗
PubMed1998

Structure of a highly acidic O-specific polysaccharide of lipopolysaccharide of Pseudoalteromonas haloplanktis KMM 223 (44-1) containing L-iduronic acid and D-QuiNHb4NHb.

An acidic O-specific polysaccharide was obtained by mild acid degradation of the lipopolysaccharide isolated by phenol-water extraction of Pseudoalteromonas haloplanktis strain KMM 223 (44-1). L-Iduronic acid (IdoA) was found to be a component of the polysaccharide and identified by NMR spectroscopy and after carboxyl-reduction followed by acid hydrolysis and acetylation, by GLC-MS as 2,3,4-tri-O-acetyl-1,6-anhydroidose. On the basis of 1H and 13C NMR spectroscopic studies, including 1D NOE, 2D NOESY, HSQC and HMBC experiments, the following structure of the branched pentasaccharide repeating unit of the polysaccharide was established: -->4)-beta-D-GlcpAI-(1-->4)-beta-D-GlcpAII-(1-->3)-beta-D-++ +QuipNHb4NHbII- (1-->2)-alpha-L-IdopA-(-->4 increases 1 alpha-D-QuipNAc4NAcI where QuiNAc4NAc and QuiNHb4NHb are 2,4-diacetamido-2,4,6-trideoxyglucose and 2,4,6-tri-deoxy-2,4- di[(S)-3-hydroxybutyramido]glucose, respectively. This is the first report of L-iduronic acid in a lipopolysaccharide and of D-QuiNHb4NHb in nature.

Carbohydrate Sequence↗
PubMed1998

Prostaglandin E1 suppresses tumor necrosis factor-alpha and interleukin-10 production by lipopolysaccharides-stimulated mononuclear cells.

Prostaglandin E1 has been clinically used in a variety of vascular occlusive diseases. We investigated the in vitro effect of prostaglandin E1 on the synthesis of tumor necrosis factor-alpha, interleukin-1, interleukin-6, interleukin-10 and transforming growth factor beta by human peripheral blood mononuclear cells stimulated with lipopolysaccharides. Prostaglandin E1 significantly suppressed both the mRNA expression and the production of tumor necrosis factor-alpha and interleukin-10 by lipopolysaccharides-stimulated peripheral blood mononuclear cells in a dose-dependent manner (1 x 10(-6)-1 x 10(-8) M). Since tumor necrosis factor-alpha is a potent proinflammatory cytokine involved in certain inflammatory diseases, our findings suggest the possibility to expand the clinical application of prostaglandin E1.

Adult↗
PubMed1999

Activation of nuclear factor-kappaB by lipopolysaccharide in mononuclear leukocytes is prevented by inhibitors of cytosolic phospholipase A2.

In monocytes, lipopolysaccharide induces synthesis and activity of the 85-kDa cytosolic phospholipase A2. This enzyme releases arachidonic acid and lyso-phospholipids from membranes which are metabolized to eicosanoids and platelet-activating-factor. These lipid mediators increase activity of transcription factors and expression of cytokine genes indicating a function for cytosolic phospholipase A2 in signal transduction and inflammation. We have shown previously that trifluoromethylketone inhibitors of cytosolic phospholipase A2 suppressed interleukin-1beta protein and steady-state mRNA levels in human lipopolysaccharide-stimulated peripheral blood mononuclear leukocytes. In this study, the subcellular mechanisms were analyzed by which trifluoromethylketones interfere with gene expression. We found that they reduced the initial interleukin-1beta mRNA transcription rate through prevention of degradation of inhibitor-kappaB alpha. Consequently, cytosolic activation, nuclear translocation and DNA-binding of nuclear factor-kappaB were decreased. Trifluoromethylketones ameliorate chronic inflammation in vivo. Thus, this therapeutic potency may reside in retention of inactive nuclear factor-kappaB in the cytosol thereby abrogating interleukin-1beta gene transcription.

Animals↗
PubMed1999

Functional expression of the fractalkine (CX3C) receptor and its regulation by lipopolysaccharide in rat microglia.

Functional expression of CX3CR1, a recently discovered receptor for the chemokine fractalkine, was investigated in cultured rat microglia. Reverse transcriptase polymerase chain reaction (PCR) experiments show abundant expression of fractalkine receptor mRNA in microglia. mRNA expression of fractalkine was undetectable in astrocytes and microglia but was very strong in cortical neurons. Incubation of microglia with lipopolysaccharide (100 ng/ml) transiently suppressed expression of fractalkine receptor mRNA. Fractalkine induced a concentration-dependent (10(-10)-10(-8) M) and, at high concentrations, oscillatory mobilization of intracellular Ca2+ in microglia The concentration-response curve of fractalkine was shifted to the right after 12 h incubation with lipopolysaccharide. It is concluded that treatment with endotoxin downregulates expression of fractalkine receptor mRNA in rat microglia and suppresses the functional response to fractalkine.

Animals↗
PubMed1999

Inhibition of interleukin-12 production in lipopolysaccharide-activated macrophages by curcumin.

Pharmacological control of interleukin-12 production may be a key therapeutic strategy for modulating immunological diseases dominated by type-1 cytokine responses. In this study we investigated the effects of curcumin (1,7-bis[4-hydroxy-3-methoxyphenyl]-1, 6-heptadiene-3,5-dione) on the production of interleukin-12 from mouse macrophages stimulated with lipopolysaccharide. Curcumin potently inhibited the production of interleukin-12 in a dose-dependent manner. The effect of curcumin on interleukin-12 p40 promoter activation was analyzed by transfecting RAW264.7 monocytic cells with p40 promoter/reporter constructs. The repressive effect mapped to a region in the p40 promoter containing a binding site for nuclear factor kappaB (p40-kappaB). Furthermore, activation of macrophages by lipopolysaccharide resulted in markedly enhanced binding activity to the kappaB site, which significantly decreased upon addition of curcumin. These results suggest that curcumin-induced inhibition of interleukin-12 production in macrophages may explain some of the biological effects of curcumin including its anti-inflammatory activity.

Animals↗
PubMed2000

Wortmannin inhibits activation of nuclear transcription factors NF-kappaB and activated protein-1 induced by lipopolysaccharide and phorbol ester.

Whether all inflammatory agents activate nuclear transcription factors NF-kappaB and activated protein-1 (AP-1) through the same mechanism is not known. We examined the effect of the phosphatidylinositol-3-kinase (PI-3K) inhibitor wortmannin on the activation of NF-kappaB and AP-1 by different inflammatory agents. Wortmannin blocked NF-kappaB and AP-1 activation by lipopolysaccharide and phorbol ester but had minimal effect on activation by hydrogen peroxide, ceramide, okadaic acid and tumor necrosis factor. Inhibition of NF-kappaB correlated with abrogation of the degradation of IkappaBalpha and of NF-kappaB-dependent reporter gene transcription. Thus, the mechanism of NF-kappaB and AP-1 activation by lipopolysaccharide and phorbol ester involves PI-3K.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1999

Helicobacter pylori lipopolysaccharide enhances the expression of NADPH oxidase components in cultured guinea pig gastric mucosal cells.

Recently, we showed that cultured guinea pig gastric pit cells possess a phagocyte NADPH oxidase-like activity, which was up-regulated by Helicobacter pylori lipopolysaccharide. We demonstrate here that these cells express all of the phagocyte NADPH oxidase components (gp91-, p22-, p67-, p47-, and p40-phoxes). Treatment with lipopolysaccharide increased the expression of gp91-, p22-, and p67-phoxes, but not that of p47- and p40-phoxes. Intriguingly, the p67-phox expression consistently correlated with up-regulation of superoxide anion-producing ability. Thus, the gastric pit cell NADPH oxidase may play an important role in regulation of the inflammatory response associated with H. pylori infection.

Animals↗
PubMed1991

A comparison of central nervous lesions directly induced by Escherichia coli lipopolysaccharide in piglets, calves, rabbits and mice.

To evaluate the role of endotoxin during Gram-negative bacterial meningitis, the nervous lesions of piglets, calves, rabbits and mice were compared by direct inoculation of Escherichia coli lipopolysaccharide into the central nervous system. Suppurative leptomeningitis was induced in piglets by small doses of lipopolysaccharide. Mice also had a mild suppurative inflammation in the leptomeninges. In contrast, calves showed suppurative pachymeningitis, but no lesions in the leptomeninges. Leptomeningeal inflammation was not induced in rabbits. Induction of the leptomeningitis by endotoxin was compared with sensitivity to intravenous or intraperitoneal endotoxin in these species.

Animals↗
PubMed1998

Changes in the lungs of lambs after intratracheal injection of lipopolysaccharide from Pasteurella haemolytica A1.

Ten lambs aged 8 weeks were inoculated intratracheally through the tracheal wall with lipopolysaccharide from Pasteurella haemolytica A1 and examined in chronological sequence by light and electron microscopy for pulmonary lesions. An acute fibrinopurulent pneumonia was produced, which resolved within 72 h but bore many resemblances to field cases of pneumonic pasteurellosis. Sequestration of neutrophils in the capillaries of the lungs and aggregation of surfactant in the alveoli occurred rapidly, followed by swelling of the alveolar and capillary endothelia, oedema, haemorrhage, and emigration of neutrophils into the interstitium and small air spaces of the lungs. Necrosis of isolated neutrophils was a constant feature. Alveolar, interstitial and intravascular macrophages and lymphoid cells increased slowly to become the predominant inflammatory cells at 72 h. A surprising feature was the transient appearance of multinucleated cells in the lungs at 2 and 6 h after inoculation. It is concluded that lipopolysaccharide makes a major contribution to the pathogenesis of P. haemolytica infection in the lungs of sheep.

Animals↗
PubMed2001

A reduction of tumor necrosis factor-alpha in paw exudate of lipopolysaccharide treated rats by nimesulide.

TNF-alpha is considered to play a pivotal role in many inflammatory and illness states. In our previous study we found that nimesulide, a COX-2 selective inhibitor, prevents the lipopolysaccharide-induced elevation in plasma TNF-alpha in rats. The present study was undertaken to elucidate the effect of nimesulide on TNF-alpha levels in the paw exudate of rats pretreated with lipopolysaccharide (LPS). Rats were injected (subplantar) with LPS (100 microg/paw) in the right hind, which resulted in a prominent increase in paw exudate TNF-alpha levels, peaked at one hour post injection. In rats pretreated with nimesulide (30 mg/kg, i.p.), the elevation in TNF-alpha in the paw exudate was significantly reduced, as compared to the LPS treated group. These results further stress the multiple antiinflammatory effects of nimesulide.

Animals↗
PubMed2000

Spatiotemporal induction patterns of cytokine and related immune signal molecule mRNAs in response to intrastriatal injection of lipopolysaccharide.

The brain's response to a direct immune challenge was examined by in situ hybridization histochemistry. Lipopolysaccharide (bacterial endotoxin) injected acutely into rat striatum induced mRNA expression for inhibitory factor kappaBalpha, interleukin (IL)-1beta, tumor necrosis factor-alpha, IL-6, IL-12 p35, inducible nitric oxide synthase, IL-1 receptor antagonist, and the type 1 IL-1 receptor. Expression patterns were evaluated at select time points ranging from 15 min to 3 days post-injection. Rats injected with vehicle alone were used to control for mechanical effects. Following lipopolysaccharide administration, a wave of mRNA induction within brain parenchyma radiated outward from the injection site, generally peaking in intensity at the 16-h time point. The individual profiles of cytokine mRNA induction patterns reveal that the brain's immune response to local inflammatory stimulation is quite elaborate and in many ways resembles the progression of cytokine induction customary of localized inflammation in peripheral tissues.

Animals↗
PubMed2000

Spatiotemporal induction patterns of cytokine and related immune signal molecule mRNAs in response to intrastriatal injection of lipopolysaccharide.

The brain's response to a direct immune challenge was examined by in situ hybridization histochemistry. Lipopolysaccharide (bacterial endotoxin) injected acutely into rat striatum induced mRNA expression for inhibitory factor kappaBalpha, interleukin (IL)-1beta, tumor necrosis factor-alpha, IL-6, IL-12 p35, inducible nitric oxide synthase, IL-1 receptor antagonist, and the type 1 IL-1 receptor. Expression patterns were evaluated at select time points ranging from 15 min to 3 days post-injection. Rats injected with vehicle alone were used to control for mechanical effects. Following lipopolysaccharide administration, a wave of mRNA induction within brain parenchyma radiated outward from the injection site, generally peaking in intensity at the 16-h time point. The individual profiles of cytokine mRNA induction patterns reveal that the brain's immune response to local inflammatory stimulation is quite elaborate and in many ways resembles the progression of cytokine induction customary of localized inflammation in peripheral tissues.

Animals↗
PubMed1997

Analysis of B7-1 and B7-2 costimulatory ligands in cultured mouse microglia: upregulation by interferon-gamma and lipopolysaccharide and downregulation by interleukin-10, prostaglandin E2 and cyclic AMP-elevating agents.

Recent evidence indicates that membrane-bound costimulatory molecules of the B7 family are important for T-cell activation and are upregulated in IFN gamma-stimulated human microglia and in multiple sclerosis active lesions. In this study we have performed a detailed analysis of B7-1 and B7-2 expression and regulation in cultured mouse glial cells using immunocytochemical and semi-quantitative reverse transcriptase-polymerase chain reaction techniques. In an immortalized mouse microglial cell line (BV-2), expression of B7-1 and B7-2 was enhanced by interferon-gamma (IFN gamma). IFN gamma was a weak inducer of B7-2 mRNA and immunoreactivity in microglia primary cultures obtained from the neonatal mouse brain, whereas lipopolysaccharide, tumour necrosis factor-alpha, colony-stimulating factors and interleukin-1 beta did not affect microglial B7-2 expression. Combined IFN gamma and lipopolysaccharide treatment very effectively upregulated the B7-2 gene expression and immunoreactivity in microglia, but not in astrocytes. In both glial cell types, expression of B7-1 was not induced by any of the above agents. Among known microglia/macrophage deactivators, interleukin-10, prostaglandin E2 and cAMP-elevating agents, but not transforming growth factor-beta 1 and interleukin-4, inhibited B7-2 transcripts and immunoreactivity in IFN gamma/LPS-stimulated microglia, thus suggesting possible paracrine and autocrine mechanisms for regulating the expression of this important T-cell costimulatory signal in the brain.

Animals↗
PubMed2003

Extraction methods for lipopolysaccharides from Escherichia coli ATCC 25922 for quantitative analysis by capillary electrophoresis.

Lipopolysaccharides (LPS) are major constituents of the cell wall of Gram-negative bacteria. Capillary zone electrophoresis (CZE) was applied to distinguish between lipopolysaccharides extracted from Escherichia coli ATCC 25922 with various techniques. Extraction methods proposed by Westphal and Jann [Methods Carbohydr. Chem. 5 (1965) 83], Galanos et al. [Eur. J. Biochem. 9 (1969) 245], Ni Eidhin and Mouton [FEMS Microbiol. Lett. 110 (1993) 133] and Nichols [Infect. Immun. 62 (1994) 3753] for LPS preparation were evaluated. Electrophoresis buffers with varying pHs were applied to assess the structure stability of the extracted LPS samples. Variations in structural breakdown were apparent demonstrating that different extraction methods removed different LPS molecules. Furthermore, the results obtained proved the CZE useful as an analytical technique for LPS evaluation. The LPS removed with the Nichols extraction procedure presented a unique electrophorogram that could in future be applied in the rapid identification of Gram-negative foodborne pathogens.

Electrophoresis, Capillary↗
PubMed1987

Enhancement of neutrophil adherence to isolated rat liver sinusoidal endothelial cells by supernatants of lipopolysaccharide-activated monocytes. Role of tumor necrosis factor.

Supernatants of endotoxin-activated monocytes have been shown to stimulate human neutrophil adherence to rat liver sinusoidal endothelial cells 3-4-fold. Evidence will be presented that tumor necrosis factor (TNF) is responsible for this phenomenon: (a) in high-performance gel filtration of supernatants of lipopolysaccharide-activated monocytes, neutrophil adhesion-inducing activity coeluted with TNF activity measured in the L929 cell-lysing assay at 25-45 kDa; (b) anti-TNF antibody treatment of supernatants of activated macrophages abolished their adhesion-inducing activity; (c) human recombinant TNF alpha stimulated neutrophil adhesion to sinusoidal endothelial cells in a dose-dependent manner. In addition, polymyxine B sulfate, which was capable of neutralizing direct effects of lipopolysaccharide on neutrophil adhesion, could abolish neither the neutrophil-adhesion-inducing activity of the supernatants of endotoxin-activated monocytes nor the effect of human recombinant TNF itself. The neutrophil-adhesion-inducing activity was due both to a direct activation of neutrophils and to an influence of the sinusoidal endothelium itself by TNF: pretreatment of sinusoidal endothelial cells with TNF followed by thorough washing resulted in an increased neutrophil attachment. Protein synthesis by endothelial cells was not required. However, incubation of sinusoidal endothelium with TNF followed by anti-TNF antibody treatment abrogated the increased neutrophil adhesion. This suggests that TNF bound to sinusoidal endothelial cell surfaces was responsible for neutrophil adhesion. It is concluded that TNF by increasing granulocyte sticking to the endothelial lining of the liver sinusoids may play a significant role in endotoxin-induced inflammation of the liver as it is found in the septic state.

Animals↗
PubMed2000

Paclitaxel causes mouse splenic lymphocytes to a state hyporesponsive to lipopolysaccharide stimulation.

Multiple immune system actions have been ascribed to paclitaxel (taxol), a novel anticancer drug, including the capacity to induce macrophage antitumor cytotoxic molecule production. In the present studies, we demonstrated that paclitaxel produced a selective inhibition of lipopolysaccharide (LPS)-induced B cell proliferation. Similarly, in vitro polyclonal antibody-forming cell responses also were found to be inhibited by paclitaxel. Conversely, paclitaxel exhibited no inhibitory effects on concanavalin A (Con A)-induced T cell proliferation. To study the pathway leading to paclitaxel-induced immunosuppression, we analyzed Raf-1/ERK and JNK/p38 MAPK pathways, both of which have been reported to be involved in LPS signaling. Our results indicate that taxol treatment inhibits Raf-1 kinase activation while having no effect on ERK activation suggesting that ERK activation is distinct from upstream Raf-1 kinase in taxol-induced immunomodulation. Furthermore, paclitaxel pretreatment caused down-regulation of stress-activated MAPKs, JNK and p38 MAPK in lipopolysaccharide (LPS)-stimulated mouse splenic lymphocytes, demonstrating that spleen cells are induced to a state hyporesponsive to LPS stimulation by pre-exposing them to paclitaxel. Taken together, these results suggest that down-regulation of JNK/p38 MAP kinase may contribute to paclitaxel-induced immunosuppression in mouse splenic lymphocytes.

Animals↗