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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new approach has been developed to circumvent the problems of false positive reactions in the Limulus Amoebocyte Lysate (LAL) assay for lipopolysaccharide (LPS) in root surface materials. These LAL-reactive materials include thrombin, thromboplastin, ribonuclease, ribonucleic acid, lipoteichoic acid and peptidoglycan fragments. In the present study, hot phenol/water extraction of these substances followed by ultracentrifugation of the resulting aqueous phases reduced their concentrations to very low levels. Furthermore, the application of Polymyxin B/Sepharose 4B affinity chromatography to these extracts enabled their intrinsic LAL-activity to be determined. Use of these techniques to assay root surface materials has identified LPS as being the major LAL-reactive material present. The mean LPS yield for the periodontally involved teeth was 4.13 micrograms/tooth, representing 2.82 micrograms/root. In contrast, the mean yield of LPS for the periodontally uninvolved teeth was 3.12 ng/tooth.
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PMID:Identity of limulus amoebocyte lysate-active root surface materials from periodontally involved teeth. 346 18

An equine antiserum to core lipopolysaccharide was produced by inoculation of 6 horses with a boiled cell bacterin made from the J-5 mutant of Escherichia coli O111:B4. The antiserum immunoglobulin G titer to J-5 mutant E coli, as determined by enzyme-linked immunosorbent assay, was 1:15,006. Pooled serum prepared before inoculation (preimmune serum) had a J-5 immunoglobulin G titer of 1:350. The J-5 antiserum was tested for its protective efficacy in sublethal endotoxemia in 14 horses. Four horses served as nontreated controls and were given nothing before endotoxin challenge exposure (10 micrograms/kg of body weight, IV). Pooled preimmune serum (3 ml/kg, IV) was administered to 5 horses and J-5 antiserum (3 ml/kg, IV) was administered to 5 other horses 2 to 15 hours before endotoxin challenge exposure. During the 24 hours postendotoxin challenge exposure, endotoxemia was accompanied by significant (P less than 0.05) time-related changes in temperature, heart rate, pulse character, respiratory rate and character, capillary refill time, mucous membrane color, fecal composition, attitude, PCV, total plasma protein, WBC count, platelet count, plasma fibrinogen, prothrombin time, activated partial thromboplastin time, fibrinolytic degradation products, plasma glucose, and plasma lactate in all horses. There were no apparent treatment vs time interactions (P greater than 0.05). Two horses (1 control and 1 given J-5 antiserum) died suddenly from unknown causes immediately after endotoxin challenge exposure. Seemingly, equine antiserum to core lipopolysaccharide did not provide protection from the adverse effects of experimental endotoxemia produced by bolus IV infusion of 10 micrograms of endotoxin/kg.
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PMID:Endotoxemia in horses: protection provided by antiserum to core lipopolysaccharide. 351 25

Lipoglycans represent a special type of lipopoly-saccharide that differs in structure from the well-known gram-negative bacteria lipopolysaccharide. After briefly describing their most important characteristics, the authors take into consideration the in vitro interaction between lipoglycans from Acholeplasma granularum, Acholeplasma oculi, and Acholeplasma axanthum and human leukocytes in terms of production of procoagulant activity. The results obtained show that the examined lipoglycans possess, similarly to lipopolysaccharides, the capacity to induce the production of procoagulant activity, thromboplastin-like, from human mononuclear cells. However, the pathophysiological significance of this endotoxin-like activity remains to be established.
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PMID:[Generation of pro-coagulation activity by leukocytes stimulated in vitro with lipoglycans from mycoplasmas]. 384 73

Experimental glomerular thrombosis was induced in rats by combined injections of nephrotoxic antiserum and lipopolysaccharide. For the development of glomerular thrombosis, administration of nephrotoxic antiserum (greater than or equal to 0.1 ml pooled material) was required as a preparatory agent and greater than or equal to 100 ng lipopolysaccharide as a provoking agent. The severity of renal lesions was not parallel with the amounts of nephrotoxic antiserum and lipopolysaccharide injected. Transient clamping of a unilateral renal artery for 10 to 20 minutes at the time of the nephrotoxic antiserum injection partially prevented the development of glomerular thrombosis in the clamped side. Intervals between the preparatory and provoking injections were found to be -4 to 72 hours for the development of renal lesions. With the preparatory injection of 0.1 to 0.3 ml nephrotoxic antiserum a thrombotic lesion developed exclusively in glomerular capillary walls greater than or equal to 2 hours after the lipopolysaccharide injection. No thrombotic lesion was observed in other tissues such as lung, liver, or intestine, but a generalized Shwartz-manlike phenomenon was observed with the preparatory injection of 0.5 ml nephrotoxic antiserum. When rats were pretreated with nephrotoxic antiserum and 3 hours thereafter transfused with 1 to 3 X 10(8) polymorphonuclear leukocytes, which had been incubated with lipopolysaccharide for 30 minutes in vitro and washed three times with buffered physiologic saline solution, a marked glomerular thrombosis was also induced. The result indicates that lipopolysaccharide plays a role in the development of thrombosis by a direct effect on leukocytes. The development of glomerular thrombosis was prevented in a leukocytopenic state when leukocyte count was less than 600/microliter, but not in thrombocytopenic rats with a platelet count 8.7 to 30 X 10(3)/microliter. Leukocyte count and plasma fibrinogen level decreased, and prothrombin time and activated partial thromboplastin time were prolonged significantly during the pathologic course. Platelet count and FDP did not change significantly. This experimental model has a basic similarity to the generalized Shwartzman reaction, but the lesions develop exclusively in glomeruli.
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PMID:Selective glomerular thrombosis in rats induced by combined injections of nephrotoxic antiserum and lipopolysaccharide. 388 61

This experiment was designed to establish a model for the study of gastrointestinal disturbances as a result of prolonged endotoxin uptake in the horse. The hepatic portal vein of 7 horses was catheterized (through flank incisions) to give chronic hepatic portal infusions of lipopolysaccharide (LPS, endotoxin). Lipopolysaccharide was infused at a rate of 1 microgram/kg of body weight/hr for 24 hours. Two of the horses were infused with saline solution for 12 hours before LPS infusions were given. Lipopolysaccharide was shown to affect behavior and hematologic and coagulation values. The 1st hour was critical for the LPS-infused horses; yet by 4 hours, the horses had apparently become refractory to continued infusion of LPS. During the 1st hour, all horses collapsed without an accompanying hypotension. A decrease in polymorphonuclear leukocytes (neutrophils) was seen during this time and was accompanied by a shortening of the recalcification tests, 1-stage prothrombin time, and activated partial thromboplastin time. There was an increased concentration of circulating fibrinogen/fibrin degradatory products. All of the LPS-infused horses showed signs of hoof discomfort and either stood with the 4 feet together beneath the body or continually shifted their weight from one front foot to the other. Hoof temperature decreased approximately 3 degrees (C) during this time and remained decreased for the duration of the experiment.
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PMID:Alterations in coagulation and hemograms of horses given endotoxins for 24 hours via hepatic portal infusions. 389 67

Monkey (Macaca fuscata) mononuclear leukocytes were stimulated to produce thromboplastin (tissue factor) upon exposure to lipopolysaccharide, LPS. The stimulation was dose-related in the concentration range of 10(-5) to 10(-1) micrograms/ml of LPS. Lipid A portion of the LPS molecule was essential to induce the leukocyte ability for tissue factor generation. Thus, a lipid-lipid interaction between LPS and the cells is a plausible trigger for eliciting the ability. Approximately 50% of the tissue factor thus produced appeared to be located on the cell surface, at which the coagulation cascade is probably initiated via the activation of factor VII. Among monkey mononuclear cell populations, monocytes were responsible for LPS-induced tissue factor production. Lymphocytes amplified the basal ability of monocytes to produce the factor by two-fold at physiological lymphocyte-monocyte ratios of 8:1 to 10:1. This indicates a complementary effect of lymphocytes upon the LPS-mediated monocyte ability. The medium supernatant from LPS-stimulated lymphocytes affected the monocyte competence while the stimulated lymphocytes did not. This result suggests that a soluble product of lymphocytes, i.e., lymphokine-like mediator, but not the cellular entity, participates in LPS-induced tissue factor production of monocytes.
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PMID:Monocyte thromboplastin (tissue factor): complementary effect of lymphocytes upon its generation by endotoxin-stimulated monkey (Macaca fuscata) cells. 403 Jul 40

Bacterial infection is associated with disseminated intravascular coagulation and fibrin deposition in the microcirculation; the mechanism of these effects in humans is still unclear. We have studied the generation of procoagulant activity (PCA) by cultured human endothelial cells (EC) in response to endotoxin. Cells from umbilical cord veins were grown in Eagle's minimum essential medium with 20% fetal calf serum till confluence. Absence of fibroblasts and macrophages was carefully checked. Endotoxin (Salmonella enteritidis lipopolysaccharide (LPS) W or Escherichia coli 0111:B4 LPS W, 0.01-1.0 micrograms/ml) was added to culture dishes for 4-6 h. PCA of EC was measured by a one-stage clotting assay and/or a two-stage amidolytic assay with the chromogenic substrate S-2222. In the absence of endotoxin, EC generated little, if any PCA (2-5 units/10(5) cells). In contrast, the addition of endotoxin resulted in generation of strong PCA that reached a maximum within 4-6 h (185-241 units/10(5) cells) and was dose-dependent between 1 and 0.01 microgram endotoxin/ml of culture medium. The generation of PCA required RNA and protein synthesis but did not require the presence of serum. No activity was found in the culture medium. The activity was of tissue thromboplastin type, as indicated by biological and immunological criteria. These endotoxin effects were observed in the absence of endothelial damage, as shown by phase-contrast microscopy and lack of 51Cr release. These data could contribute to elucidate the pathogenesis of vascular complications associated with endotoxemia in man.
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PMID:Cultured human endothelial cells generate tissue factor in response to endotoxin. 634 90

Alveolar macrophages are thought to participate in the clearance of fibrin from the injured lung, but their ability to facilitate the conversion of fibrinogen to fibrin (procoagulant activity) has not been described. In order to characterize their procoagulant properties, unstimulated alveolar macrophages obtained from normal rabbits were tested for their ability to accelerate the coagulation of plasma in a one-stage clotting assay. Compared with control assays containing no macrophages (coagulation times greater than 500 s), intact cells (10(6)/ml) were shown to display procoagulant activity (coagulation time, 153.6 +/- 11.3 s mean +/- SEM). Cell lysis caused further procoagulant activity to be expressed (125.6 +/- 11.8 s). Alveolar macrophages that were stimulated in vitro with bacterial lipopolysaccharide (LPS) or the purified complement fragments C5a and C5a des Arg caused further significant (p less than 0.002) reductions in coagulation times (intact cells, 71 to 76 s; lysed cells, 27 to 32 s), representing 5- to 6-fold and 30- to 40-fold increases in the procoagulant activity of intact and lysed cells, respectively. The generation of this material was independent of the presence of lymphocytes. The procoagulant material was identified as a cell-associated tissue thromboplastin, acting via the extrinsic coagulation pathway. These findings show that alveolar macrophages have procoagulant activity that is markedly augmented by LPS and complement fragments. This suggests that alveolar macrophages may contribute to intra-alveolar fibrin deposition in vivo.
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PMID:Procoagulant activity of rabbit alveolar macrophages. 634 42

We demonstrated previously that rabbit alveolar macrophages stimulated in vitro by bacterial lipopolysaccharide (LPS) have markedly enhanced procoagulant activity (PCA), caused by increased production of a cell-associated tissue thromboplastin. The present study examined the role of arachidonic acid metabolites in modulating the expression of this PCA. Alveolar macrophages lavaged from normal rabbits were incubated in vitro with LPS, indomethacin, and purified prostaglandins, and the resultant PCA was measured. LPS stimulated a significant increase in macrophage PCA relative to unstimulated controls (p less than 0.01). Indomethacin suppressed the ability of LPS to stimulate PCA in a dose-related fashion. The addition of PGE2 or PGE1 reversed the suppressive action of indomethacin (p less than 0.01), whereas PGF2 alpha, PGD2, TXB2, and 6-keto PGF1 alpha had no such effect. PGE2 did not affect PCA unless the macrophages were also stimulated with LPS. A significant correlation (rs = 0.72, p less than 0.01) existed between the level of LPS-stimulated macrophage PCA and the corresponding amount of immunoreactive PGE2 released into the culture medium. The results of this study demonstrate that PGE is required for the LPS-mediated enhancement of rabbit alveolar macrophage-associated tissue thromboplastin and that PGE can stimulate the expression of PCA by appropriately conditioned cells.
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PMID:Prostaglandin E is required for the augmentation of procoagulant activity of LPS-stimulated rabbit alveolar macrophages. 658 Dec 28

Tissue factor (TF) is a transmembrane receptor which, in association with factors VII and VIIa, activates factor IX and X, thereby activating the coagulation protease cascades. In response to bacterial lipopolysaccharide (LPS) monocytes transcribe, synthesize and express TF on their surface. We investigated whether LPS-induced TF in human monocytes is mediated by protein kinase C (PKC) activation. The PKC agonists phorbol 12-myristate 13-acetate (PMA) and phorbol 12, 13 dibutyrate (PdBu) were both potent inducers of TF in human monocytes, whereas 4 alpha-12, 13 didecanoate (4 alpha-Pdd) had no such effect. Both LPS- and PMA-induced TF activity were inhibited, in a concentration dependent manner, by three different PKC inhibitors: H7, staurosporine and calphostin C. TF antigen determination confirmed that LPS-induced cell-surface TF protein levels decreased in parallel to TF functional activity under staurosporine treatment. Moreover, Northern blot analysis of total RNA from LPS- or PMA-stimulated monocytes showed a concentration-dependent decrease in TF mRNA levels in response to H7 and staurosporine. The decay rate of LPS-induced TF mRNA evaluated after the arrest of transcription by actinomycin D was not affected by the addition of staurosporine, suggesting that its inhibitory effect occurred at a transcriptional level. We conclude that LPS-induced production of TF and its mRNA by human monocytes are dependent on PKC activation.
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PMID:Endotoxin-induced tissue factor in human monocytes is dependent upon protein kinase C activation. 1101 86


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