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

Fluid transport across cultures of bovine tracheal epithelium was measured with a capacitance probe technique. Baseline fluid absorption (Jv) across bovine cells of 3.2 microliter. cm-2. h-1 was inhibited by approximately 78% after 1 h of exposure to suspensions of Pseudomonas aeruginosa, with a concomitant decrease in transepithelial potential (TEP) and increase in transepithelial resistance (Rt). Effects of P. aeruginosa were blocked by amiloride, which decreased Jv by 112% from baseline of 2.35 +/- 1.25 microliter. cm-2. h-1, increased Rt by 101% from baseline of 610 +/- 257 Omega. cm2, and decreased TEP by 91% from baseline of -55 +/- 18.5 mV. Microelectrode studies suggested that effects of P. aeruginosa on amiloride-sensitive Na absorption were due in part to a block of basolateral membrane K channels. In the presence of Cl transport inhibitors [5-nitro-2-(3-phenylpropylamino)-benzoic acid, H2-DIDS, and bumetanide], P. aeruginosa induced a fluid secretion of approximately 2.5 +/- 0.4 microliter. cm-2. h-1 and decreased Rt without changing TEP. However, these changes were abolished when the transport inhibitors were used in a medium in which Cl was replaced by an impermeant organic anion. Filtrates of P. aeruginosa suspensions had no effect on Jv, TEP, or Rt. Mutants lacking exotoxin A or rhamnolipids or with defective lipopolysaccharide still inhibited fluid absorption and altered bioelectrical properties. By contrast, mutations in the rpoN gene encoding a sigma factor of RNA polymerase abolished actions of P. aeruginosa. In vivo, changes in transepithelial salt and water transport induced by P. aeruginosa may alter viscosity and ionic composition of airway secretions so as to foster further bacterial colonization.
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PMID:Pseudomonas aeruginosa induces changes in fluid transport across airway surface epithelia. 981 77

Early systemic arterial hypotension is a common clinical feature of Pseudomonas septicemia. To determine if Pseudomonas aeruginosa endotoxin induces the release of endothelium-derived nitric oxide (EDNO), an endogenous nitrovasodilator, segments of canine femoral, renal, hepatic, superior mesenteric, and left circumflex coronary arteries were suspended in organ chambers (physiological salt solution, 95% O2/5% CO2, pH 7.4, 37 degrees C) to measure isometric force. In arterial segments contracted with 2 microM prostaglandin F2 alpha, Pseudomonas endotoxin (lipopolysaccharide (LPS) serotype 10(Habs) from Pseudomonas aeruginosa (0.05 to 0.50 mg/ml) induced concentration-dependent relaxation of segments with endothelium (P < 0.05) but no significant change in tension of arteries without endothelium. Endothelium-dependent relaxation in response to Pseudomonas LPS occurred in the presence of 1 microM indomethacin, but could be blocked in the coronary artery with 10 microM NG-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of nitric oxide synthesis from L-arginine. The inhibitory effect of L-NMMA on LPS-mediated vasorelaxation of the coronary artery could be reversed by exogenous 100 microM L-arginine but not by 100 microM D-arginine. These experiments indicate that Pseudomonas endotoxin induces synthesis of nitric oxide from L-arginine by the vascular endothelium. LPS-mediated production of EDNO by the endothelium, possibly through the action of constitutive nitric oxide synthase (NOSc), may decrease systemic vascular resistance and may be the mechanism of early hypotension characteristic of Pseudomonas septicemia.
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PMID:Endothelium-dependent vasodilation in response to Pseudomonas aeruginosa lipopolysaccharide: an in vitro study on canine arteries. 987 5

In 24-h water- and food-deprived rats, we have evaluated the effects of cromoglycate sodium salt, an inhibitor of the mast cell degranulation with anti-inflammatory and membrane-stabilizating activity, on the central effects induced by Escherichia coli lipopolysaccharide (LPS). Intraperitoneal (i.p.) injection of LPS (0.25, 0.50 and 1 mg/kg) induced a dose-dependent inhibition of water and food intake, fever, reduction in locomotor activity as well as increased anxiety levels. All these LPS effects were antagonized by a prior intracerebroventricular (i.c.v.) injection of cromoglycate sodium salt (100, 150 and 200 microg/rat). Our findings suggest that peripheral LPS administration may activate brain mast cells and indicate an involvement of these cells in brain pathophysiology.
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PMID:Central effects of cromoglycate sodium salt in rats treated with lipopolysaccharide. 1007 11

The relationship between nitric oxide (NO) and blood pressure (BP) in deoxycorticosterone acetate-salt hypertensive rats (DOC) was investigated. Although urinary NO2- + NO3- (NOx) excretion (UNOxV) increased 2 weeks after surgery (2W-DOC), UNOxV decreased 4 weeks after surgery (4W-DOC) compared with that of the control. BP and UNOxV did not change in DOC after treatment with L-arginine (Arg-DOC). Aorta from 4W-DOC and Arg-DOC had significantly decreased relaxation responses to acetylcholine. Deendothelialized aorta from 4W-DOC and Arg-DOC had significantly decreased relaxation responses to lipopolysaccharide. These data suggest that: 1) transient increase of NO synthesis is accompanied by elevation of BP, but long-term elevation of BP decreases NO synthesis in endothelium and smooth muscle cells; 2) L-arginine supplement has no effect on the development of hypertension nor on NO production by endothelium and smooth muscle cells in DOC.
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PMID:[The role of nitric oxide in deoxycorticosterone acetate-salt hypertensive rats]. 1036 18

We have determined the effects of the following factors on the resistance of Gram-negative bacteria against nisin and curvacin A: (i) chemotype of the lipopolysaccharide (LPS), (ii) addition of agents permeabilizing the outer membrane, (iii) the fatty acid supply of the growth medium, and (iv) the adaptation to acid and salt stress. Bacteriocin activity was determined against growing and resting cells as well as protoplasts. All smooth strains of Escherichia coli and Salmonella enterica serovar Typhimurium were highly resistant towards the bacteriocins, whereas mutants that possess the core of the LPS, but not the O antigen, as well as deep rough LPS mutants were sensitive. Antibiotics with outer membrane permeabilizing activity, polymyxin B and polymyxin B nonapeptide, increased the sensitivity of smooth E. coli towards nisin, but not that of deep rough mutants. Incorporation of 1 g l(-1) of either oleic acid or linoleic acid to the growth media greatly increased the susceptibility of E. coli LTH1600 and LTH4346 towards bacteriocins. Both strains of E. coli were sensitive to nisin and curvacin A at a pH of less than 5.5 and more than 3% (w/v) NaCl. Adaptation to sublethal pH or higher NaCl concentrations (pH 4.54 and 5.35 or 4.5% (w/v) NaCl) provided only limited protection against the bacteriocidal activity of nisin and curvacin A. Adaptation to 4.5% (w/v) NaCl did not result in cross protection to bacteriocin activity at pH 4.4, but rendered the cells more sensitive towards bacteriocins.
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PMID:Resistance of Escherichia coli and Salmonella against nisin and curvacin A. 1037 33

We purified three proline-rich antimicrobial peptides from elastase-treated extracts of sheep and goat leukocytes and subjected two of them, OaBac5alpha and ChBac5, to detailed analysis. OaBac5alpha and ChBac5 were homologous to each other and to bovine Bac5. Both exhibited potent, broad-spectrum antimicrobial activity under low-concentration salt conditions. While the peptides remained active against Escherichia coli, Pseudomonas aeruginosa, Bacillus subtilis, and Listeria monocytogenes in 100 mM NaCl, they lost activity against Staphylococcus aureus and Candida albicans under these conditions. ChBac5 was shown to bind lipopolysaccharide, a property that could enhance its ability to kill gram-negative bacteria. Proline-rich Bac5 peptides are highly conserved in ruminants and may contribute significantly to their innate host defense mechanisms.
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PMID:Purification and properties of proline-rich antimicrobial peptides from sheep and goat leukocytes. 1041 80

Neutrophil-mediated organ damage is a common feature of many disease states. We previously demonstrated that resuscitation with hypertonic salt solutions prevented the endotoxin-induced leukosequestration and consequent lung injury, and this effect was partially attributed to an altered surface expression of adhesion molecules, CD11b and L-selectin. In this study we investigated the mechanisms whereby osmotic stress evokes L-selectin shedding. The metalloprotease inhibitor RO 31-9790 prevented the osmotic down-regulation of L-selectin, indicating that this process was catalyzed by the same "sheddase" responsible for L-selectin cleavage induced by diverse inflammatory stimuli. The trigger for hypertonic shedding was cell shrinkage and not increased osmolarity, ionic strength, or intracellular pH. Volume reduction caused robust tyrosine phosphorylation and its inhibition by genistein and erbstatin abrogated shedding. Shrinkage stimulated tyrosine kinases Hck, Syk, and Pyk2, but prevention of their activation by the Src-family inhibitor PP1 failed to affect the L-selectin response. Hypertonicity elicited the Src family-independent activation of p38, and the inhibition of this kinase by SB203580 strongly reduced shedding. p38 was also essential for the N-formyl-methionyl-leucyl-phenylalanine- and lipopolysaccharide-induced shedding but not the phorbol ester-induced shedding. Thus, cell volume regulates L-selectin surface expression in a p38-mediated, metalloprotease-dependent manner. Moreover, p38 has a central role in shedding induced by many inflammatory mediators.
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PMID:Cell volume-dependent regulation of L-selectin shedding in neutrophils. A role for p38 mitogen-activated protein kinase. 1041 35

Bovine aortic endothelial cells produce prostacyclin as their major arachidonic acid metabolite. cAMP, in turn, is the second messenger for prostacyclin. In the present study, we investigated the effects of cAMP-elevating agents on prostacyclin production by bovine aortic endothelial cells. Treatment of resting bovine aortic endothelial cells with cAMP-elevating agents inhibited prostacyclin production and cyclooxygenase activity, without affecting arachidonic acid release. No change was detected in cyclooxygenase-1 protein expression. The specific inhibitor of protein kinase A, Rp-cAMPS (adenosine 3',5'-cyclic monophosphorothioate, Rp-isomer, triethylammonium salt), and the phosphatase inhibitor, okadaic acid, both suppressed cAMP-induced inhibition, suggesting that this inhibition is mediated by a phosphorylation-dephosphorylation cascade, which is possibly protein kinase A-dependent. In lipopolysaccharide-treated cyclooxygenase-2 expressing bovine aortic endothelial cells, where cyclooxygenase-1 activity was selectively inhibited, dibutyryl cAMP failed to inhibit cyclooxygenase-2 activity. Cyclooxygenase-2 protein was induced upon treatment with dibutyryl cAMP and further induction of cyclooxygenase-2 protein was effected by IBMX (3-isobutyl-1-methyl-xanthine) and dibutyryl cAMP in bacterial lipopolysaccharide-stimulated cells. These results suggest that increased cellular cAMP selectively inhibits cyclooxygenase-1 activity without altering cyclooxygenase-1 protein expression, and at the same time, up-regulates cyclooxygenase-2 protein. This complex regulation of cyclooxygenase activity and protein expression by cAMP may represent a prostacyclin-induced autoregulatory mechanism in bovine aortic endothelial cells.
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PMID:Differential regulation of cyclooxygenase isoenzymes by cAMP-elevating agents. 1047 33

In this study the authors give immunocytochemical evidence for the presence of interleukin (IL)-1alpha- and tumour necrosis factor (TNF) alpha-like molecules in the haemocytes of last instar larvae from the greater wax moth Galleria mellonella. Similar results are demonstrated in a continuous haemocyte line (BTI-EA-1174-A) from the salt marsh caterpillar Estigmene acraea. In Galleria mellonella larvae granular cells show a strong positive reaction with both primary antibodies, whereas plasmatocytes are stained to a lesser extent. Cell line haemocytes also react positively with both antibodies. After activating the cells with lipopolysaccharide (LPS) staining of Estigmene acraea cells is decreased, whereas Galleria mellonella haemocytes show no visible reaction in comparison to non-activated cells.
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PMID:Presence of IL-1- and TNF-like molecules in Galleria mellonella (Lepidoptera) haemocytes and in an insect cell line Fromestigmene acraea (Lepidoptera). 1047 99

Endotoxemia leads to cytokine-mediated alterations of the hepatocellular sodium-taurocholate-cotransporting polypeptide (ntcp). We hypothesized that stimulated macrophages are essential transducers for down-regulating hepatocellular bile salt uptake in response to endotoxin (lipopolysaccharide [LPS]) exposure. Using an in vitro model, we exposed mouse macrophages (IC-21 cell line) to LPS for 24 hours. Concentrations of cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6 increased 10.6-fold, 12.5-fold, and 444-fold, respectively, in LPS-conditioned IC-21 medium (CM) versus unconditioned IC-21 medium (UM). WIF-B rat hepatoma hybrid cells were incubated with either CM or UM or treated directly with medium containing recombinant TNF-alpha, IL-1beta, and IL-6. [(3)H]Taurocholate ([(3)H]TC) uptake decreased in WIF-B cells exposed to either TNF-alpha (54% of control), IL-1beta (78%), IL-6 (55%) as single additives, or in triple combination (TCC) (43%). A virtually identical decrease was observed after exposing WIF-B cells to CM (52%, P <.001). LPS had no direct effect on [(3)H]TC uptake. CM treatment did not decrease L-alanine transport in WIF-B cells. Blocking antibodies against TNF-alpha, IL-1beta, and IL-6 restored the diminished [(3)H]TC uptake in cells exposed to TCC and CM to 87% and 107% of controls, respectively. Northern blotting revealed that ntcp messenger RNA (mRNA) expression was significantly reduced in WIF-B cells after exposure to CM, and in primary rat hepatocytes exposed to CM or TNF-alpha (68%, 14%, and 29% of control, respectively). We conclude that macrophages and their ability to secrete the cytokines TNF-alpha, IL-1beta, and IL-6 may be essential in mediating the endotoxin-induced cholestatic effect of decreased hepatocellular bile salt uptake.
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PMID:Endotoxin-stimulated macrophages decrease bile acid uptake in WIF-B cells, a rat hepatoma hybrid cell line. 1061 37


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