SEARCH · PubMed Health

Results for “LIPOPOLYSACCHARIDES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources

PubMed1990

Effects of Escherichia coli lipopolysaccharide on nitrate synthesis and on nitrosation of proline in rats.

Male Ola:SD rats were fed purified diets containing 5 or 20% lactalbumin as the protein source, with or without concomitant administration of Escherichia coli lipopolysaccharide (50-250 micrograms/kg, ip), and changes in 24-hr urinary nitrate excretion, plasma urea, plasma-nitrate pool size and 24-hr urinary nitrosoproline excretion were measured. Urinary nitrate and urinary 14C-nitrosoproline excretion (after oral [14C]proline administration) were significantly greater for rats receiving the high-protein diet compared with those on the low-protein diet. The co-administration of lipopolysaccharide increased nitrate excretion in both diet groups (although the increase was greatest (relatively) in the animals fed 5% lactalbumin), but did not significantly alter urinary nitrosoproline excretion by either group. Plasma urea concentrations and plasma-nitrate pool size were increased by a high-protein diet and/or lipopolysaccharide administration. These findings suggest that treatments which alter the availability of nitrate in vivo are not necessarily associated with increased nitrosation of proline.

Animals↗

PubMed1993

Lipopolysaccharide induces fever and decreases tail flick latency in awake rats.

In humans, somatic aches and pains are frequently reported during fever. To determine whether exogenous pyrogen administration increases nociceptive responsiveness in rats, the tail flick reflex evoked by noxious heat was compared in animals that received an intraperitoneal injection of exogenous pyrogen (lipopolysaccharide) or vehicle (saline). There were no differences in skin temperature between lipopolysaccharide- and vehicle-injected rats. Awake rats injected with lipopolysaccharide exhibited an increase in colonic temperature and a decrease in tail flick latency when compared to vehicle-injected rats. Neural events that trigger fever may therefore also modulate nociceptive responsiveness.

Animals↗

PubMed1994

Interleukin-1 receptor type I mRNA in mouse brain as affected by peripheral administration of bacterial lipopolysaccharide.

Following administration of endotoxin in vivo, alterations of interleukin-1 (IL-1) receptor binding have been reported. In order to assess in vivo regulation of IL-1 receptor gene expression in brain, mRNA levels for IL-1 receptor type I were measured after peripheral administration of bacterial lipopolysaccharide in mice. When 25 micrograms of lipopolysaccharide were administered intraperitoneally, IL-1 receptor type I mRNA in the brain was increased after 3 h. After 20 h, the level was diminished. This result suggests that bacterial lipopolysaccharide affects regulation of IL-1 receptor type I mRNA expression in mouse brain.

Animals↗

PubMed1978

The 4-amino sugars present in the lipopolysaccharides of vibro cholerae and related vibrios.

Brief treatment, with 10 M hydrochloric acid, of the lipopolysaccharides of Vibrio cholerae and related organisms led to the release of 4-amino-4, 6-dideoxy-D-mannose (D-perosamine) and 4-amino-4-deoxyl-L-arabinose. These sugar are highly unstable and undergo complex changes in neutral and basic media. Of the strains examined, the lipopolysaccharides from representatives of the Inaba group contain only D-perosamine, while those of the Ogawa biotype have 4-amino-4-deoxyl-L-arabinose as an additional component. The other Vibrios produce lipopolysaccharides which lack these sugars.

Amino Sugars↗

PubMed1992

The acute inflammatory response to lipopolysaccharide in CNS parenchyma differs from that in other body tissues.

Acute inflammation is important for defence against infection, wound repair and the mediation of auto-immune tissue destruction. Myelomonocytic recruitment in acute inflammation is a stereotyped and non-specific response to tissue insult which begins within 2 h. In this study, lipopolysaccharide was injected into the murine CNS and other body sites of mice to compare the inflammatory responses. Doses of lipopolysaccharide which induced typical myelomonocytic recruitment in skin and the choroid plexus had no effect in CNS parenchyma, apart from the morphological activation of local resident microglia. The CNS parenchymal response proceeded independently of that in the choroid plexus-cerebral ventricles and had three distinct and unique phases. Initially there was minimal neutrophil exudation and a two-day delay before any increase in macrophage-microglial cell number. Next, there was a rapid increase in macrophage-microglial cell numbers during the third day, mainly due to recruitment of blood monocytes. During this phase, leukocyte recruitment was restricted to monocytes which rapidly adopted the arborized microglial phenotype. Monocytes migrated through an intact blood-brain barrier independent of changes in solute permeability. Finally, there was a florid myelomonocytic reaction predominantly in the white matter, one week after intracerebral injection of 2 micrograms lipopolysaccharide. At this time, the leukocyte reaction disrupted the blood-brain barrier, mononuclear phagocytes expressed macrophage morphology and abundant major histocompatibility complex Class II antigen, and T lymphocytes were present. Myelomonocytic entry into the CNS was partially inhibited by prior blockade of the type 3 complement receptor, known to mediate leukocyte adhesion to endothelium elsewhere. The processes which lead to rapid myelomonocytic recruitment in other tissues are absent in CNS parenchyma. Understanding the molecular mechanisms responsible could have considerable significance both for CNS pathophysiology as well as possible anti-inflammatory therapeutic application elsewhere in the body.

Animals↗

PubMed1991

Identification of 3-deoxy-lyxo-2-heptulosaric acid in the core region of lipopolysaccharides from Rhizobiaceae.

A 3-deoxy-2-heptulosaric acid (DHA), very probably with the lyxo-configuration, was identified in the R-core region of lipopolysaccharides from nodulating strains of Rhizobium leguminosarum, Rhizobium meliloti and from all three biovars of the phytopathogenic Agrobacterium tumefaciens. Its structure could be deduced from the fragmentation pattern of the corresponding alditol acetates obtained after reduction of the 2-keto and the 1.7-carboxy groups by sodium borohydride or sodium borodeuteride. DHA in lipopolysaccharide was not destroyed by periodate and is therefore not in a terminal position. Two DHA-containing oligosaccharides, namely glucosyl (1----4)-3-deoxy-2-heptulosaric acid and rhamnosyl-rhamnosyl-(1----5)-3-deoxy-2-heptulosaric acid could be tentatively identified by mass spectrometric methods amongst the products of mild acidic hydrolysis of lipopolysaccharides of Rhizobium leguminosarum strain 24. The two types of non-nodulating mutants of Rhizobium leguminosarum included in this study did not contain 3-deoxy-2-heptulosaric acid.

Carbohydrate Sequence↗

PubMed1988

Cytidine 5'-monophospho-N-acetyl neuraminic acid and a low molecular weight factor from human blood cells induce lipopolysaccharide alteration in gonococci when conferring resistance to killing by human serum.

Recently evidence has been obtained that a minute amount of cytidine 5'-monophospho-N-acetyl neuraminic acid (CMP-NANA) or a closely related compound is the low Mr factor in human red blood cells which induces Neisseria gonorrhoeae (BS4(agar] to resistance to killing by fresh human serum. Induction of gonococci to resistance by both CMP-NANA and semi-purified low Mr factor from red blood cells was accompanied by a 35-55% reduction of silver staining of lipopolysaccharide separated in SDS-PAGE gels of proteinase K digests. These alterations in lipopolysaccharide are probably responsible for conferring serum resistance. However, lipopolysaccharide-containing digests from resistant as well as from susceptible gonococci neutralised serum bactericidal activity. These observations may have wider implications since CMP-NANA is a sialylating agent wide-spread in mammalian tissues and LPS is ubiquitous amongst Gram-negative pathogens.

Antibodies, Bacterial↗

PubMedDate not supplied

Characterization of smooth Brucella lipopolysaccharides and polysaccharides by monoclonal antibodies.

Two mouse monoclonal antibodies (mAb) generated to the M antigen of Brucella melitensis 16M were analysed. Binding profiles of both monoclonals were established by a competitive enzyme-linked immunosorbent assay using chemically defined lipopolysaccharides, O polysaccharides and native hapten polysaccharides from B. melitensis 16M, B. abortus 544 and Yersinia enterocolitica O:9. Using this assay, significant differences in the reactivity of both antibodies were found with A and M antigens from Brucella spp. and the O polysaccharide from Y. enterocolitica O:9. These findings are consistent with the simultaneous expression of A and M epitopes on the lipopolysaccharide of all smooth Brucella strains. Quantitatively similar inhibitory powers were established for the native hapten and O polysaccharide from B. melitensis 16M. However, different behaviour was observed between both antigenic preparations obtained from B. abortus 544. The use of lipopolysaccharide-M-specific mAb in different serological tests instead of polyclonal antisera may be of great practical use for minimizing the risk of the appearance of cross-serological reactions between smooth Brucella strains and Y. enterocolitica O:9.

Antibodies, Monoclonal↗

PubMed1995

Kinetics of nitric oxide synthase induction by Propionibacterium avidum and lipopolysaccharide.

Conditions for the induction of rat liver Ca2(+)-independent nitric oxide synthase were determined with killed Propionibacterium avidum, and compared with lipopolysaccharide endotoxin. Similar maximal induction was obtained intraperitoneally with the two types of inducers but killed Propionibacterium avidum gave a long-lasting induction while lipopolysaccharide displayed a rapid and short response. Moreover, the induction resulting from an intravenous administration of killed Propionibacterium avidum reached 60 times that of the control whereas lipopolysaccharide treatment induced a 24-fold stimulation only. It is noteworthy that with the first inducer the nitric oxide activity was stable with time whereas with the second one it dropped after 8 h. Whatever the route of administration of killed Propionibacterium avidum, some huge vacuolated Kupffer cells were found in the liver whose parenchyma was almost normal. Numerous monocytes, and unaltered Kupffer cells, were observed. Kupffer cells were identified to be responsible for the uptake of killed Propionibacterium avidum.

Animals↗

PubMed1995

Lipopolysaccharide interferes with the induction of peripheral T cell death.

In mice injected with superantigens, T cells specific for that antigen proliferate and then die. It has been suggested that the target cells die because they encounter superantigen on the surfaces of nonprofessional presenting cells, such as B cells, which cannot deliver costimulatory signals to T cells. A number of reagents that induce costimulatory molecules on B cells were tested. Lipopolysaccharide very effectively prevented T cell death driven by superantigen. Perhaps surprisingly, the action of lipopolysaccharide was not mediated through the expected costimulatory molecule, B7. Rather, the effects of lipopolysaccharide involved the production of inflammatory cytokines, in particular TNF alpha. The rescued cells survived in vitro culture and were resistant to Fas-induced killing. These data demonstrate that LPS can block antigen-induced T cell death perhaps by interfering with Fas signaling.

Animals↗

PubMed2003

Substitution pattern of 3-deoxy-D-manno-oct-2-ulosonic acid in bacterial lipopolysaccharides investigated by methylation analysis of whole LPS.

3-Deoxy-D-manno-oct-2-ulosonic acid (Kdo) is a constituent of the inner core part of bacterial lipopolysaccharides (LPS). This sugar may contribute to biological activities of the LPS, the type of substitution of Kdo is thus of importance and this work is aimed at the evaluation of a method for monitoring the substitution of Kdo in LPS. The procedure consists of three steps, namely permethylation of the lipopolysaccharide, with iodomethane and sodium methylsulfinylmethanide or NaOH in Me(2)SO, or with methyl triflate, then the product is methanolysed with HCl in MeOH and acetylated with acetic anhydride in pyridine. The resulting partially methylated acetates of Kdo methyl glycosides were analyzed by gas-liquid chromatography-electron impact ionization mass spectrometry (GLC-MS). For several derivatives of Kdo, specific GLC retention times and MS fragmentation patterns were determined. Lipopolysaccharides from several bacterial strains were isolated and analyzed with three different methods of methylation. The complete solubilization of the LPS in the acid form allows diminishing possible undermethylation. Sodium methylsulfinylmethanide is the most efficient agent in the permethylation of the whole LPS, of all the tested procedures. Methylation with methyl triflate allows the detection of base labile substituents on Kdo residues.

Chromatography, Gas↗

PubMed2005

Ca2+-dependent K+ channels are targets for bradykinin B1 receptor ligands and for lipopolysaccharide in the rat aorta.

Although rat aorta smooth muscle cells in culture constitutively express bradykinin B1 receptors, the normotensive rat aorta does not respond to the bradykinin B1 receptor agonist des-Arg9-bradykinin, whereas vessels from the spontaneously hypertensive rat (SHR) respond to bradykinin B1 receptor agonists with cell membrane hyperpolarization and relaxation. Bacterial lipopolysaccharide also is inactive on the normotensive rat but hyperpolarizes the SHR aorta. To determine whether this could be due to the increased intracellular Ca2+ concentration ([Ca2+]i) in the SHR, we raised [Ca2+]i in normotensive rats by treatment with thapsigargin. In the thapsigargin-treated aorta, both lipopolysaccharide and des-Arg9-bradykinin induced hyperpolarization, which was reversed by the Ca2+-dependent K+ channel inhibitor iberiotoxin and by the bradykinin B1 receptor antagonists Lys-[Leu8]-des-Arg9-bradykinin and [Leu8]-des-Arg9-bradykinin. Thus the bradykinin B1 receptor, as well as lipopolysaccharide, needs activated Ca2+-dependent K+ channels for functional expression. The two bradykinin B1 receptor inhibitors, however, have effects on Ca2+-dependent K+ channels which are not mediated by bradykinin B1 receptors.

Animals↗

PubMed2004

Testosterone influenced the expression of Notch1, Notch2 and Jagged1 induced by lipopolysaccharide in macrophages.

Testosterone plays an extensive role in modulating macrophages functions in mammals. In this study, we incubated murine bone marrow macrophages which were positive to the surface antigen F4/80 with lipopolysaccharide and increasing amounts of testosterone. Expression of Notch family members (including Notch1, Notch2 and Jagged1) was investigated at transcription and post-transcription levels through RT-PCR and Western blotting assay followed by densitometric analyses. Results showed that testosterone influenced the lipopolysaccharide-induced expression of Notch1, Notch2 and Jagged1 in macrophages. The elevated expression of Notch1 and Notch2 induced by lipopolysaccharide was repressed by testosterone at lower levels, but enhanced at higher hormone levels. In addition, the expression of Jagged1 was enhanced by various amounts of testosterone. These results suggest that testosterone affected the expression of Notch family members in activated macrophages.

Animals↗

PubMed2004

Oral arginine reduces gut mucosal injury caused by lipopolysaccharide endotoxemia in rat.

BACKGROUND: The objective of this study was to evaluate the effects of lipopolysaccharide (LPS) endotoxemia and enteral arginine (ARG) supplementation on intestinal structural changes, enterocyte proliferation, and apoptosis in rat. METHODS: Male Sprague-Dawley rats, weighing 250-280 g, were divided into three experimental groups: control rats, LPS rats treated with lipopolysaccharide given ip at a dose of 10 mg/kg every 24 h (two injections), and LPS-ARG rats treated with enteral arginine given in drinking water (2%) 72 h before and following injection of LPS. Intestinal structural changes, enterocyte proliferation, and enterocyte apoptosis were determined on day 3 following the first LPS injection. RESULTS: LPS rats demonstrated a significant decrease in bowel weight in duodenum, mucosal weight in duodenum, jejunum, and ileum, mucosal DNA and protein in jejunum and ileum, and villus height in jejunum and ileum compared to control animals. LPS rats also had a significantly lower cell proliferation index in jejunum and ileum and a higher apoptotic index in jejunum and ileum compared to control rats. LPS-ARG animals demonstrated greater duodenal bowel weight, duodenal and ileal mucosal weight, ileal mucosal DNA and protein, ileal villus height, and jejunal and ileal cell proliferation index compared to LPS animals. CONCLUSIONS: LPS endotoxemia impairs the integrity of the gastrointestinal mucosa in rat. Decreased cell proliferation and increased apoptosis may be considered the main mechanisms responsible for the decreased cell mass. Enteral arginine administration decreases the mucosal injury caused by lipopolysaccharide.

Administration, Oral↗

PubMed2004

Lipopolysaccharide-induced pulmonary inflammation is not accompanied by a release of anandamide into the lavage fluid or a down-regulation of the activity of fatty acid amide hydrolase.

The effect of lipopolysaccharide inhalation upon lung anandamide levels, anandamide synthetic enzymes and fatty acid amide hydrolase has been investigated. Lipopolysaccharide exposure produced a dramatic extravasation of neutrophils and release of tumour necrosis factor alpha into the bronchoalveolar lavage (BAL) fluid, which was not accompanied by epithelial cell injury. The treatment, however, did not change significantly the levels of anandamide and the related compound palmitoylethanolamide in the cell-free fraction of the BAL fluid. The activities of the anandamide synthetic enzymes N-acyltransferase and N-acylphosphatidylethanolamine phospholipase D and the activity of fatty acid amide hydrolase in lung membrane fractions did not change significantly following the exposure to lipopolysaccharide. The non-selective fatty acid amide hydrolase inhibitor phenylmethylsulfonyl fluoride was a less potent inhibitor of lung fatty acid amide hydrolase than expected from the literature, and a dose of 30 mg/kg i.p. of this compound, which produced a complete inhibition of brain anandamide metabolism, only partially inhibited the lung metabolic activity.

Acyltransferases↗

PubMed1996

Inflammatory cytokine (interleukins 1, 6 and 8 and tumor necrosis factor-alpha) release from cultured human fetal membranes in response to endotoxic lipopolysaccharide mirrors amniotic fluid concentrations.

OBJECTIVE: This study was conducted to quantitate and compare the amount of cytokines released from human fetal membranes in response to treatment with bacterial lipopolysaccharide and to compare this with amniotic fluid levels. STUDY DESIGN: Amniochorionic membranes were collected from women undergoing elective repeat cesarean section and showing no signs of infection- or pregnancy-related complications. Membranes were maintained in an organ explant system and stimulated with bacterial lipopolysaccharide for 24 hours. Media samples were collected and stored at -20 degrees C until cytokine levels were assayed by enzyme-linked immunosorbent assay. RESULTS: Enzyme-linked immunosorbent assay results demonstrated that lipopolysaccharide stimulated production of interleukins 1, 6 and 8 and tumor necrosis factor-alpha by the fetal membranes in comparison with the control cultures. A greater release of interleukin-6 and interleukin-8 compared with interleukin-1 and tumor necrosis factor-alpha was noticed. The relationships between cytokine concentrations observed in culture mirror those seen in amniotic fluid. CONCLUSION: Amniochorionic membranes can respond to an infectious process with increased secretion of interleukins 1, 6 and 8 and tumor necrosis factor-alpha. Cytokines produced from both amnion and chorion (interleukin-6 and interleukin-8) are released in greater quantities than those cytokines produced from chorion or amnion alone (interleukin-1 and tumor necrosis factor-alpha). These studies support a major role for amnion in infection-induced preterm labor.

Amniotic Fluid↗

PubMed1996

Repeated administration of low-dose lipopolysaccharide induces preterm delivery in mice: a model for human preterm parturition and for assessment of the therapeutic ability of drugs against preterm delivery.

OBJECTIVE: Our purpose was to establish a new animal model for human preterm delivery for assessment of the protective effect of drugs against preterm delivery. STUDY DESIGN: C3H/HeN, C3H/HeN, and BALB/c female mice impregnated by C3H/HeN, B6D2F1, and B6D2F1 male mice, respectively, were treated intraperitoneally with Escherichia coli lipopolysaccharide (0 to 100 microgram/kg, single dose or repeated doses at 1- to 6-hour intervals) on days 12 through 17 of pregnancy. On day 15 of pregnancy, the C3H/HeN females that had been impregnated by B6D2F1 males and administered lipopolysaccharide were treated intraperitoneally with indomethacin (1000 microgram/kg), ritodrine hydrochloride (1000 microgram/kg), urinary trypsin inhibitor (25 x 10(4) units/kg), or gabexate mesylate (100 mg/kg); preterm or term delivery was recorded for these mice. RESULTS: C3H/HeN females impregnated by B6D2F1 males revealed the highest (100%) incidence of preterm delivery when the females were treated with 50 microgram/kg lipopolysaccharide twice at a 3-hour interval on day 15 or 17 of pregnancy. Indomethacin and urinary trypsin inhibitor used separately significantly decreased the incidence of preterm delivery, but only urinary trypsin inhibitor, and not any of the other drugs, significantly increased the incidence of term delivery in the mice. CONCLUSION: A new animal model for investigation of preterm delivery was established, and its usefulness for assessment of the protective effect of drugs against preterm delivery was demonstrated.

Animals↗

PubMed1996

Induction and posttranslational expression of cytokines in a first-trimester trophoblast cell line by lipopolysaccharide.

OBJECTIVES: The response to infection by human first-trimester trophoblasts is a poorly understood event. This study was undertaken to determine whether first-trimester trophoblasts are capable of responding to an infection stimulus and mediating an immune response. STUDY DESIGN: HTR-8/SVneo cells were exposed to lipopolysaccharide (1 microgram/ml) or media alone for either 0, 2, 4, 6, 8, or 24 hours. Northern analysis was conducted by use of a panel of antisense cytokine probes. Enzyme-linked immunosorbent assays specific for either interleukin-1 alpha, interleukin-6, interleukin-8, or transforming growth factor-beta 1 were conducted on corresponding cell culture supernatants, and the kinetics of expression were determined. RESULTS: Interleukin-1 alpha, interleukin-6, interleukin-8, and transforming growth factor-beta 1 transcription occurred maximally between 2 and 8 hours of culture in media containing lipopolysaccharide, with a subsequent diminution of response. Enzyme-linked immunosorbent assay analysis corroborated lipopolysaccharide induction seen at the level of transcription, with significant posttranslational expression of these cytokines being detected between 2 and 24 hours in culture (p < 0.01). CONCLUSIONS: Expression of the proinflammatory cytokines interleukin-1 alpha, interleukin-6, interleukin-8 and transforming growth factor-beta 1 strongly support the contention that human first-trimester trophoblasts are capable of responding to an infection stimulus and eliciting an immune response through cytokine-based immune signaling.

Blotting, Northern↗