UNIPROT:P43026 - FACTA Search

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

The route of excretion of lipopolysaccharide (LPS) and its possible degradation in vivo was studied in rats using biosynthetically radiolabelled LPS from Salmonella abortus equi, carrying 3H activity exclusively in fatty acids and 14C activity in fatty acids and sugars. Following intravenous injection of the above LPS in AS2 rats with or without anaesthesia, excretion of radioactivity occurred mainly in the faeces and to smaller extent in urine. The rate of excretion was slow, a large part of the radioactivity being still present in the liver after 14 days. In faeces the percent recovery of 3H (18%) was lower than that of 14C (32%) suggesting loss of tritium activity and thereby of fatty acids from the excreted LPS. A similar loss of tritium was also found in the material remaining in the liver and spleen 14 days after LPS administration. In urine the material recovered during 14 days (about 7% of injected) was different from the original LPS, 70% of 14C activity being dialysable and practically all 3H activity being volatile. Similar results were also obtained following administration of the LPS intraperitoneally under anaesthesia. However, when the LPS was administered intraperitoneally without anaesthesia, in the majority of the animals, 90% of 14C and 54% of 3H was excreted in faeces within 3 days, suggesting that both route of administration and use of anaesthesia during injection influence the subsequent rate of excretion of LPS.
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PMID:Excretion of radioactivity in faeces and urine of rats injected with 3H,14C-lipopolysaccharide. 400 48

The intravenous injection of 10 microgram of a lipopolysaccharide extracted from E. Coli to rabbits leads to the appearance of a hypotensive effect for des-Arg9-BK and increases significantly the vasodilator effect of this peptide in isolated hearts and its contractile effects in strips of large arteries and veins. LPS elicits these responses when administered 5 or 20 h before anesthesia; the hypotensive response of animals receiving LPS just before anaesthesia is similar to that of untreated rabbits. All actions of des-Arg9-BK in vivo, in isolated hearts and in isolated tissues are blocked by des-Arg10,[Leu9]-kallidin (KD), a specific inhibitor of kinins B1-receptor. These data are taken as evidence of the appearance of B1-response to kinins in the few hours following LPS injection. The response of the animals, perfused organs and isolated tissues to other agonists, such as substance P or [Tyr(Me)8]-BK (an activator of B2-receptors for kinins) are not affected by the treatment with LPS nor are they modified by the antagonist des-Arg10,[Leu9]-KD. The present data, together with previous studies on the sensitization mechanism of B1-receptor containing preparations, suggest that LPS induces the formation of B1-receptors in the rabbit, within a few hours. The activation of B1-receptors by des-Arg9-BK produces hypotension, coronary vasodilation and stimulation of large arteries and veins isolated and suspended in vitro. Some large arteries and veins (e.g. the aorta and the anterior mesenteric vein) as well as some peripheral vascular beds (e.g. the coronary vessels) have the ability of generating B1-receptors, while other organs (e.g. the external jugular vein) have not or very little. The reason for this phenomenon as well as the intimate mechanism by which LPS induces the formation of B1-receptors remain to be elucidated.
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PMID:Induction of beta 1-receptors for kinins in the rabbit by a bacterial lipopolysaccharide. 611 53

A murine corneal scratch model has been used extensively to study various aspects of the pathogenesis of Pseudomonas aeruginosa, a common etiologic agent of corneal infections. This model uses mild inhalation anesthetics which keep the animals immobile for a relatively short time and promote the interaction between the infecting organisms and the corneal wound. Under these circumstances, only a small number of P. aeruginosa isolates delivered at inocula of > 10(7) CFU are infectious. We determined that this model is useful for studying other P. aeruginosa strains given at lower doses if injectable anesthetics are administered prior to infection to keep the animals immobile for 15 to 30 min. Under these conditions, eight clinical isolates of P. aeruginosa tested at doses of 10(8) CFU per eye induced corneal perforation and/or phthisis in C3H/HeN mice. The 50% infective doses of several strains were between 3 x 10(2) and 1 x 10(5) CFU per mouse eye. When this modified anesthetic procedure was used to evaluate the roles of different P. aeruginosa virulence factors in eye infections, pathology was not observed when eyes were inoculated with 10(8) CFU of strains deficient in production of a complete lipopolysaccharide or the RpoN sigma factor. A strain with a point mutation in the fur gene, involved in production of iron-regulated factors, showed decreased virulence, while a mutant deficient in both hemolytic and nonhemolytic phospholipase C was fully virulent. By modifying the anesthesia procedure, the corneal scratch model allows rapid evaluations of the roles of P. aeruginosa virulence factors in corneal infections.
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PMID:Rapid and sensitive method for evaluating Pseudomonas aeruginosa virulence factors during corneal infections in mice. 764 83

The hypothesis was tested that alcohol may modulate alveolar macrophage cytokine receptors, thus interfering in lung immune defense mechanisms. Male rats were treated with alcohol either acutely (7 hr continuous intravenous alcohol infusion at a rate of 30 mg/100 g body weight/hr after a priming dose of 175 mg/100 g body weight) or chronically (feeding an alcohol-containing liquid diet for 12-14 weeks). Three hr before killing, the rats received an intravenous injection of Gram-negative bacterial lipopolysaccharide (LPS; Escherichia coli, O26:B6, 100 micrograms/100 g body weight). After anesthesia with sodium pentobarbital, the trachea was cannulated, and the lungs excised and lavaged to obtain alveolar macrophages. The recovered cells were used to measure the binding of recombinant human [125I]tumor necrosis factor-alpha (TNF-alpha) and [125I]interleukin-6 (IL-6). Kd and Bmax were determined at 4 degrees C, thus reflecting only the cell-surface binding sites and their affinity. Two binding sites were detected for both cytokines: high-affinity (Kd1 in the range of 20-110 pM), low-capacity (Bmax1 in the range of 1-13 fmol/10(6) cells), and low-affinity (Kd2 in the range of 0.6-1.3 nM), high-capacity (Bmax2 in the range of 34-100 fmol/10(6) cells). Acute alcohol treatment significantly decreased Bmax1 (39%) and Bmax2 (79%) for TNF-alpha, whereas chronic alcohol feeding abrogated the Bmax1 (Bmax1 = 0), without affecting Bmax2. In the acute group, LPS had an effect similar to that of alcohol. Alcohol administration did not modify the LPS effects. The following changes were monitored for IL-6 binding. Acute alcohol treatment markedly reduced (86%) Bmax2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression of tumor necrosis factor-alpha and interleukin-6 cell-surface receptors of the alveolar macrophage in alcohol-treated rats. 769 40

Multisystem organ failure (MSOF) is the major cause of late death following trauma. The gut is hypothesized to be the source of an ongoing systemic inflammatory response that drives MSOF. It has also been suggested that while a single physiologic insult might not reliably cause MSOF, the addition of a delayed second stress will. This is known as the "two-hit" theory. The purpose of this study was to investigate the two-hit theory by observing the hemodynamic and bacteriologic response to a second stress in a subacute pig model of hemorrhagic and endotoxic shock. Swine (n = 18, 30-40 kg) were fed an antibiotic-free diet for 14 days. During instrumentation and experimentation on days 1 and 3, all animals were anesthetized (ketamine, isofluorane). On day 1, all animals had placement of central venous and arterial catheters, a portal venous catheter, and superior mesenteric artery flow probe. Group E (n = 6) underwent instrumentation on day 1, then infusion of endotoxin (25 mcg/kg E. coli lipopolysaccharide) on day 3. Group HE (n = 7) underwent instrumentation then hemorrhagic shock (mean arterial pressure = 40 mm Hg for 4 hours) on day 1, then infusion of endotoxin on day 3. Group H (n = 5) were instrumented and hemorrhaged on day 1, and underwent anesthesia only on Day 3. Between periods of anesthesia the animals were allowed food and water ad lib and systemic blood was sampled for culture every 12 hours. On day 5, the animals were euthanized prior to organ sampling for bacterial culture. One animal from group HE died during endotoxic shock on day 3.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic changes and gut barrier function in sequential hemorrhagic and endotoxic shock. 776 Mar 96

Guinea pigs were passively sensitized with immune serum to ovalbumin (OA), control serum, or saline. Twenty-four hours later, they inhaled aerosols of OA (2% in saline), saline, or lipopolysaccharide (LPS). Following anesthesia, bronchoalveolar lavage (BAL) was performed at 30, 60, 90 and 120 min postinhalation. Alveolar macrophages (AM) were isolated from the BAL fluid and incubated (18 h) in medium alone or with zymosan (1 mg/ml). Supernatants were collected and levels of interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) determined by bioassays. Unstimulated AM from animals that inhaled OA, saline, or LPS secreted similar amounts of IL-1 at 30, 60, and 90 min postinhalation. Zymosan (1 mg/ml) significantly increased IL-1 secretion by AM collected at 60 and 90 min from OA-sensitized animals that inhaled OA or saline. AM from guinea pigs sensitized to OA that inhaled OA or LPS secreted significantly increased amounts of IL-6 at 30, 60, 90, and 120 min postchallenge compared to saline sensitized controls. In all groups, AM from LPS-treated animals secreted large amounts of TNF-alpha at all sampling times postchallenge; AM from OA-sensitized and challenged animals secreted increasing amounts of TNF-alpha with time postchallenge, spontaneously and in response to zymosan. By contrast, AM from saline sensitized and challenged guinea pigs did not release detectable amounts of TNF-alpha spontaneously and secreted very low amounts in the presence of zymosan. These findings show that antigen challenge results in a rapid activation of AM isolated from BAL and suggest AM may initiate the development of inflammatory processes associated with antigen challenge.
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PMID:Release of monokines by pulmonary macrophages following antigen challenge in sensitized guinea pigs. 798 26

We investigated the local in vivo action of lipopolysaccharide (LPS), a potent monocyte activator, and of macrophage colony-stimulating factor (M-CSF), a hemopoietic growth factor influencing monocyte differentiation, on bone resorption in normal female 8-wk-old rats. LPS (2 injections of 0.5 microgram), M-CSF (2 injections of either 12.5, 25, 100, or 500 ng), or vehicle was injected into bone marrow space through a thin catheter implanted, under hydrochloride anesthesia, in the distal end of the right femur. Histomorphometry was performed after staining of the tartrate-resistant acid phosphatase (TRAP). The number of osteoclasts and of TRAP-positive marrow cells (considered as osteoclast precursors) were counted in the secondary spongiosa. LPS caused a 3-fold increase in osteoclast surface, a 4.5-fold increase in the number of osteoclasts, but no change in the number of TRAP-positive marrow cells. M-CSF induced a striking dose-dependent biphasic effect on the number of TRAP-positive marrow cells and on bone resorption (no change with the lowest or with the highest concentrations, although the two intermediate doses significantly increased resorption surfaces and the number of osteoclasts). Our results demonstrate a local in vivo effect of LPS and of M-CSF on bone resorption and suggest that these substances act at different stages of osteoclast development and function.
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PMID:Local bone injections of LPS and M-CSF increase bone resorption by different pathways in vivo in rats. 846 Jun 86

Although burn wound excision and grafting have been shown to improve patient survival, the effects on immune function, especially humoral immunity, are not completely understood. The purpose of this study was to investigate the effect of immediate and early wound excision on antibody synthesis and B-cell proliferation, specifically, antibody response to PGPS, a ubiquitous bacterial cell wall antigen. Thirty-six male BALB/c mice were divided into four groups. Sham mice received no burn, and remaining mice received a 30% body surface area full-thickness burn. Under general anesthesia, excision and grafting was performed either 6 or 72 hr after injury (BE&G6 and BE&G72 groups). A fourth control group received burn but did not undergo excision and grafting (Burn group). Splenocytes were isolated 8 days postburn and stimulated with 2.5 microgram/ml lipopolysaccharide. Anti-PGPS IgM, total IgM, and total IgG levels were determined by ELISA. B-cell proliferation, measured by [3H]-thymidine uptake, was expressed as stimulation index. All B-cell functions were significantly suppressed by burn injury. Immediate excision and grafting (BE&G6) restored anti-PGPS IgM synthesis to normal, while nonspecific B-cell functions did not change significantly. Early excision and grafting (BE&G72), however, failed to significantly improve any B-cell functions. Immediate but not early BE&G restored antibody synthesis to the bacterial cell wall antigen (PGPS). Immediate BE&G may therefore lead to a decrease in bacterial infection after burn injury.
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PMID:Immediate burn wound excision restores antibody synthesis to bacterial antigen. 866 Nov 90

To determine actions of acute intoxication on pathophysiologic responses to trauma, anesthetized and ventilated mongrel pigs received a 20% solution of ethanol (EtOH) by an intravenous (IV group; 2 g/kg, n = 8) or an oral (PO group; 3 g/kg, n = 12 x 60 minutes) route of administration, or the lactated Ringer's vehicle (LR group; n = 12). After 60 minutes, all were subjected to soft tissue injury and 30 to 35% hemorrhage, 60-minute shock, and then resuscitation, with shed blood plus supplemental LR. After 3 days, host defense was challenged with Escherichia coli lipopolysaccharide (LPS); (1 microgram/kg x 30-minutes IV). The supplemental resuscitation was identical (50-53 mL/kg/hours), but posttraumatic acidosis was observed in the IV group and the PO group (base deficit = 4.4 +/- 1.3 and 5.5 +/- 0.9 mEq/L) and not in the LR group. After 3 days, the acid-base equilibrium was restored, but a difference in host defense was unmasked by LPS. In the LR group, LPS-evoked pulmonary vasoconstriction was followed by decreased compliance and ventilation-perfusion mismatch, which was associated at 3 to 5 hours with a base deficit, reduced SVO2, and reduced PO2 (-0.5 +/- 0.2 mEq/L, 46 +/- 1%, 127 +/- 1 mm Hg). These changes were blunted in the PO group (2.0 +/- 0.1 mEq/L, 56 +/- 1%, 183 +/- 4 mm Hg) and potentiated in the IV group (-4.3 +/- 0.5 mEq/L, 40 +/- 2%, 60 +/- 2 mm Hg), even though more fluid was required to maintain systemic arterial and cardiac filling pressures following LPS administration in the IV (40 +/- 6 mL/kg/ hours) versus the LR or PO groups (31 +/- 5 or 23 +/- 3). The PO versus LR differences could not be attributed to enteral nutrition because an isocaloric solution of 50% dextrose had no effect versus LR solution. EtOH caused neutropenia following trauma, relative to LR solution, but the IV versus PO differences could not be discriminated on the basis of neutrophil or lymphocytes counts, nor CD18 receptor expression, nor renal or hepatic dysfunction. However, T4 lymphocytes and cortisol, a nonspecific index of inflammation, were higher for at least 24 hours after trauma with IV, relative to PO or LR. Blood EtOH was similar with IV or PO during resuscitation (100-120 mg/dL), but the kinetics were different prior to trauma. With PO, blood EtOH slowly accumulated to a steady state plateau, the level of which was higher with no anesthesia or no trauma. With IV, blood EtOH peaked at 275 mg/dL and then exponentially declined with a rate that was not influenced to a major extent by trauma or by anesthesia. Therefore: 1) EtOH absorption is impaired during trauma (in part because of reduced gut blood flow); 2) acute EtOH intoxication at the time of trauma altered neutrophils, plasma cortisol, and T4 lymphocytes during recovery and host defense to a superimposed LPS challenge. The apparently favorable effect of PO versus IV EtOH on the response to endotoxemia after trauma probably reflects differences in the kinetics of blood EtOH in the interval before reperfusion but a "first pass" effect (metabolism in the gut or liver) might also explain the data.
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PMID:Acute ethanol intoxication and endotoxemia after trauma. 867 25

Studies of cardiovascular physiology are frequently performed under barbiturate anesthesia even though the effect of barbiturates on the pressor response to catecholamines is controversial, and their effect on the response to other agonists is unknown. The effect of pentobarbital (PB) anesthesia on the pressor and heart rate (HR) dose responses to norepinephrine (NE), angiotensin II (AII), vasopressin (VP) and neuropeptide Y (NPY) was studied in vivo in normal and endotoxemic rats. Four groups of rats (5-6 rats/group) were studied for each agonist: 1) anesthetized/endotoxemic, 2) anesthetized/control, 3) conscious/endotoxemic, and 4) conscious/control. Anesthesia was maintained with 10 mg/kg of PB i.v. q 45 minutes. Endotoxemia was established by infusion of a non-hypotensive dose of E. coli lipopolysaccharide 0127:B8, (LPS, 10 micrograms/10 microliters/min) throughout the experiment. One hour after the LPS (or saline control) infusion was started, dose response curves of the pressor and HR responses to agonists were established. LPS infusion resulted in marked suppression of the pressor response to NE, AII, and VP in both conscious and anesthetized rats. LPS infusion suppressed the response to NPY in conscious, but not in anesthetized rats. LPS did not affect the baroreceptor reflex. In both normal and endotoxemic rats, PB anesthesia suppressed the pressor response and attenuated the baroreceptor reflex to AII and NPY, enhanced the pressor response without affecting the heart rate response to NE, and attenuated the baroreceptor reflex to VP. The pressor response to VP was suppressed by anesthesia in normal, but not in endotoxemic rats. PB anesthesia interferes with the cardiovascular effects of different agonists in a variable manner, depending on the agonist tested and the presence or absence of endotoxemia, indicating their different modes of action. These effects should be considered when planning in vivo experiments with these and other agonists.
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PMID:Effect of pentobarbital anesthesia on the pressor response to agonists in vivo in normal and endotoxemic rats. 874 96

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