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)

We compared the immunological responses of leukocytes taken from healthy negative controls, laboratory workers immunized with the phenol-insoluble French vaccine against brucellosis, patients acutely ill with brucellosis, and patients chronically infected with Brucella melitensis. A salt-extractable antigen (protein-rich but with traces of lipopolysaccharide) and a sonicated suspension from B. melitensis 16M were used as antigens for in vitro lymphocyte proliferation test. Quantitation of T cells showed that the ratio of CD4+/CD8+ cells decreased as the condition of the patient deteriorated. An assay to quantitate the cell-mediated immunity showed that the activities of mononuclear cells stimulated with concanavalin A increased as the disease progressed as well.
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PMID:Cell response to a salt-extractable and sonicated Brucella melitensis 16M antigen in human brucellosis. 766 86

Both tumor necrosis factor (TNF) and platelet-activating factor (PAF) are released during sepsis and are important mediators of septic lung injury. I investigated the interactions of TNF and PAF on vasoactive responses in the pulmonary circulation. In isolated rat lungs perfused with a cell- and plasma-free physiological salt solution, PAF (0.01- and 0.1-micrograms boluses) caused transient dose-dependent pulmonary arterial and venous constrictions. In vivo pretreatment of the rats with TNF (0.02 or 0.2 mg/kg i.v.) 1 h before lung isolation increased lung myeloperoxidase activity and markedly enhanced PAF-induced pulmonary vasoconstriction without affecting the pressor responses to angiotensin II or hypoxia. In contrast, pretreatment with lipopolysaccharide (10 mg/kg), which increased lung myeloperoxidase to the same extent as TNF, caused only a modest enhancement of PAF-induced vasoconstriction associated with reduced pressor responses to angiotensin II and hypoxia. Ex vivo perfusion of isolated lungs with TNF for 1 h did not affect PAF vasoconstriction. The TNF-induced potentiation of PAF vasoconstriction was not altered by depletion of circulating neutrophils with vinblastine but was blocked by Dazmegrel, a thromboxane synthase inhibitor. Thus, TNF potentiates PAF-induced pulmonary vasoconstriction by an in vivo mechanism that is neutrophil independent but thromboxane dependent. This TNF-PAF interaction likely contributes to the development of pulmonary hypertension during sepsis.
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PMID:TNF potentiates PAF-induced pulmonary vasoconstriction in the rat: role of neutrophils and thromboxane A2. 789 27

Peptidoglycan isolated from pathogenic bacteria has been previously found to exhibit various biological activities. The aim of this investigation was to evaluate the toxicity of Treponema denticola peptidoglycan towards epithelial cells. The cytotoxicity of a lipopolysaccharide-like material was also determined. Epithelial cells were incubated with the test substances and cell viability was assayed by measuring lactate dehydrogenase activity and the conversion of tetrazolium salt into blue formazan. Morphological changes in the epithelial cells were monitored by scanning and transmission electron microscopy. While lipopolysaccharide-like material exerted negligible toxic effects on the epithelial cells, peptidoglycan was highly toxic. This cytotoxicity was both time- and concentration-dependent and was higher in the presence of serum. The epithelial cells appeared to be unable to recover following a short period of incubation with peptidoglycan. The study demonstrated that peptidoglycan from T. denticola is a potent toxic factor for epithelial cells. This represents a potential new virulence factor for this suspected periodontopathogen.
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PMID:Cytotoxic effect of peptidoglycan from Treponema denticola. 801 19

In addition to participating in protein synthesis in cells and tissues, L-arginine is essential for the synthesis of urea, creatine, creatinine, nitric oxide, and agmatine and influences hormonal release and the synthesis of pyrimidine bases. This places L-arginine, its precursors and its metabolites at the center of the interaction of different metabolic pathways and interorgan communication. Thus L-arginine participates in changing the internal environment in different but simultaneous ways, ranging from disposal of protein metabolic waste, muscle metabolism, vascular regulation, immune system function, and neurotransmission, to RNA synthesis and hormone-mediated regulation of the internal milieu. In normal rats, inhibition of the nitric oxide pathway results in systemic hypertension and decreased glomerular filtration rate and effective renal plasma flow. If the inhibition of this pathway is sustained, then glomerulosclerosis and death from uremia follow. Dietary intervention with L-arginine has resulted in amelioration of a number of experimental kidney diseases, such as those caused by subtotal nephrectomy, diabetic, nephropathy, cyclosporin A administration, salt-sensitive hypertension, ureteral obstruction, puromycin amino-nucleoside nephrosis, kidney hypertrophy due to high-protein feeding, and glomerular thrombosis due to administration of lipopolysaccharide. The present review addresses the current evidence for the beneficial effects of dietary intervention with L-arginine in a number of experimental renal diseases and describes the basis for the concept of L-arginine deficiency (absolute or relative) in certain settings in which supplementation of the diet with this amino acid may be beneficial.
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PMID:Role of arginine in health and in renal disease. 809 48

Bactericidal/permeability-increasing protein (BPI) is a potent antimicrobial agent produced by polymorphonuclear leucocytes that specifically interacts with and kills Gram-negative bacteria. An 825 bp gene determining the bactericidal N-terminal domain of human BPI was chemically synthesized and expressed as inclusion bodies in Escherichia coli. The recombinant polypeptide, BPI', was solubilized and conditions under which it folded to give the active protein were determined. Folding was critically dependent on the urea and salt concentrations as well as the pH. BPI' bound with high affinity to Salmonella typhimurium cells (apparent Kd = 36 nM), permeabilized their outer membranes to actinomycin D, specifically activated a synovial fluid phospholipase A2 and showed potent bactericidal activity. In contrast with the native protein, however, it could not be efficiently released from the cell surface by the addition of high concentrations of Mg2+ ions. Pre-incubation of the protein with lipopolysaccharide or trypsin prevented cytotoxicity. However, boiling BPI' immediately before its addition to cells did not block its bactericidal activity, suggesting that it may be able to function even when presented to cells in an unfolded form. A BPI' derivative, containing a 13-residue foreign antigenic determinant genetically inserted between Ala115 and Asp116, was also produced. The derivative was functional in the above assays and bound with high affinity to S. typhimurium (apparent Kd = 74 nM). These results imply that the region defined by these residues is not involved in the lipopolysaccharide-binding or bactericidal activities of BPI. The availability of functional, nonglycosylated recombinant derivatives of BPI should greatly aid detailed studies on its structure, interactions with lipopolysaccharide and mechanism of action.
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PMID:The region around residue 115 of human bactericidal/permeability-increasing protein is not involved in lipopolysaccharide binding or bactericidal activity. Chemical synthesis and expression of a gene coding for the active domain and characterization of recombinant proteins. 814 87

We have studied the role of lipopolysaccharide (LPS) for the insertion of LPS-free porin from Paracoccus denitrificans into planar lipid bilayers and its function therein. For this, we reconstituted the porin into different asymmetric planar lipid bilayers with or without LPS and into symmetric phospholipid bilayers. LPS-free porin added to the various bilayer systems was found to induce a step-wise increase in membrane conductance with different incorporation rates, depending on the presence of LPS in the bilayer leaflet opposite to porin addition. The incorporation rate into asymmetric LPS/phospholipid membranes from the phospholipid side was more than 10-fold higher than that observed for pure phospholipid membranes. The porin formed general diffusion pores without any salt specificity. The mean single-channel conductance did not depend on the presence of LPS and was about 4.2 nS for a subphase containing 1 M KCl in all systems tested. At certain applied transmembrane voltages, which depended on membrane composition and were approximately greater than 100 mV for the LPS/phospholipid system, single-channel closing in three steps was observed. Differences in the voltage dependence of porin-channel closing could be correlated with the surface charge of the bilayer. From the voltage-dependent gating behaviour proof for an oriented incorporation of the porin molecules, depending on the side of porin addition, and evidence for their orientation could be derived. Measurements at temperatures above and below the beta<==>alpha phase transition temperature of LPS gave evidence for the influence of membrane rigidity on the gating behaviour.
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PMID:Influence of the lipid matrix on incorporation and function of LPS-free porin from Paracoccus denitrificans. 814 21

We have shown that several human malignant glioma cell lines are stimulated by bacterial lipopolysaccharide (E. coli 0111:B4, 1 microgram/ml) to produce a high molecular weight (> 200 kD) growth activity for BALB 3T3, clone A31 cells. This glioma-derived growth factor (GDGF-2) acts like a 'competence' factor. Malignant glioma cell line D-54 MG constitutively produced GDGF-2, which we have partially characterized from serum-free conditioned culture medium. GDGF-2 is resistant to heat (100 degrees C, 5 min), acidic (pH 2, 2 hr) or reducing (0.5 M 2 ME, 30 min) conditions as well as exposure to RNases; however, it is sensitive to > 4 freeze-thaw cycles, alkaline (pH 11, 2 hr) conditions or pre-treatment with proteolytic enzymes. GDGF-2 had a pl of 6.8 determined by preparative isoelectric focusing, bound to DEAE, with elution at 35 and 185 mM NaCl and at 43% acetonitrile from a C4 reversed phase column. GDGF-2 activity was not neutralized by antibodies to TGF alpha, TGF beta, PDGF, VEGF or TNF alpha indicating that it is not immunochemically related to these growth factors. However GDGF-2 co-chromatographed on Superose 12 HPLC (250 x 9 mm; 5% isopropanol, 6 mM CHAPS in PBS) with a substance that suppressed growth of mink lung epithelial cells (Mv1Lu), but not BALB 3T3 cells, and could be neutralized by anti-TGF beta antibodies. GDGF-2 activity eluted from heparin columns in 0.6 M NaCl; thus, it is not a heparin binding growth factor. D-54 MG cell line produced alpha 2-macroglobulin (alpha 2M), which is known to bind TGF beta; however, immunoprecipitation of alpha 2M did not deplete TGF beta or GDGF-2 activity. Further, neither GDGF-2 or TGF beta can be dissociated into lower molecular weight active components by chromatography in high salt (2 M NaCl) or 2-ME (0.5 M). GDGF-2 may be a novel autocrine or paracrine mitogen, stimulating mitotic division or interfering with normal cell growth regulation.
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PMID:Partial characterization of glioma-derived growth factor 2: a novel mitogenic activity from human cell line D-54 MG. 814 64

The relationship of acid adaptation to tolerance of other environmental stresses was examined in Salmonella typhimurium. S. typhimurium was adapted to acid by exposing the cells to mildly acidic conditions (pH 5.8) for one to two cell doublings. Acid-adapted cells were found to have increased tolerance towards various stresses including heat, salt, an activated lactoperoxidase system, and the surface-active agents crystal violet and polymyxin B. Acid adaptation increased cell surface hydrophobicity. Specific outer membrane proteins were induced by acid adaptation, but the lipopolysaccharide component appeared to be unaltered. These results show that acid adaptation alters cellular resistance to a variety of environmental stresses. The mechanism of acid-induced cross-protection involved changes in cell surface properties in addition to the known enhancement of intracellular pH homeostasis.
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PMID:Acid adaptation induces cross-protection against environmental stresses in Salmonella typhimurium. 832 3

Recent studies by our group suggested that lysozyme (LZM) has a high affinity for bacterial lipopolysaccharide (LPS) of both the smooth and rough forms, and inhibits various immunomodulatory activities of LPS. GLA60 is a synthetic monosaccharide analogue of bacterial lipid A, well-known as sharing large part of lipid A activities but with very low toxicity. In this study, we characterized the interaction of LZM with GLA60 in comparison to that with E. coli 0111 LPS (smooth form), taking a physicochemical approach. Using a dansylated lysozyme probe (DNS-LZM), LZM was found to bind to GLA60 in all 3 of its forms, free acid, triethylamine (TEA) salt and bovine serum albumin (BSA) complex of GLA60, as well as natural LPS. Compared with LPS, the complex formation of the TEA salt was weakly dependent on temperature and incubation time. LZM also bound to biologically inactive GLA analogues, GLA 64 and GLA69, at a high affinity, as well as to GLA 60. By using chemically modified LZM, it was found that the ionic as well as hydrophobic interactions are important for the complex formation.
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PMID:Binding of lysozyme to synthetic monosaccharide lipid A analogue, GLA60. 836 74

In the present report, we investigated suppressive effects of a naphthalene derivative, (7E)-N-(2-carboxyphenyl)-8-(2-naphthyl)-5,6-trans-5,6-methano-7- octenamide L-lysine salt (TEI-6472), on in vitro and in vivo antigen-specific IgE response. Anti-trinitrophenyl (TNP) IgE response induced in vitro in TNP-keyhole limpet hemocyanin (KLH)-primed murine spleen cells was suppressed by about 60% in the presence of 10(-6) M TEI-6472. On the other hand, anti-TNP IgG1 and IgM response were not significantly suppressed under the same conditions. Proliferative responses of BALB/c spleen cells stimulated by lipopolysaccharide, concanavalin A or allogeneic spleen cells were not inhibited by TEI-6472 at 10(-6)-10(-5) M. Interleukin 4 production from helper T-cell clone, D10.G4.1 was suppressed only slightly (less than 20%) at 10(-6) M TEI-6472. This compound was also effective in suppressing secondary anti-TNP IgE response in mice that were immunized twice with TNP-KLH and alum. When 10-20 mg/kg/day TEI-6472 was administered s.c. for 5 consecutive days starting from one day before the first and the second immunization, secondary anti-TNP IgE response was inhibited most strongly (40-45%). Anti-TNP IgG1 response was also inhibited but to a smaller extent (20-24%), while anti-TNP IgM response was suppressed only slightly (0-15%). These results suggest that, under appropriate conditions, TEI-6472 can suppress IgE responses more preferentially both in vitro and in vivo.
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PMID:Suppression of IgE antibody response in mice by a naphthalene derivative, TEI-6472. 837 39


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