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PubMed1994

Expression of the carbohydrate recognition domain of lung surfactant protein D and demonstration of its binding to lipopolysaccharides of gram-negative bacteria.

Surfactant protein D is a collagenous C-type lectin (collectin) that is found almost exclusively in the lung. A recombinant protein, composed of the neck-region and the carbohydrate binding domain of bovine lung surfactant protein D, has been overexpressed in E. coli. The recombinant protein showed the same sugar binding specificity as the native protein and was able to bind to the lipopolysaccharides of several strains of Gram-negative bacteria, such as Klebsiella pneumoniae, Pseudomonas aeruginosa and Escherichia coli, which are known to cause lung infections. The binding was calcium-dependent and was inhibited by maltose. Native bovine surfactant protein D was also shown to be able to bind to these lipopolysaccharides in the same manner.

Animals↗

PubMed1995

Lovastatin inhibits proliferation and differentiation and causes apoptosis in lipopolysaccharide-stimulated murine B cells.

Lipopolysaccharide-stimulated murine B lymphocytes were incubated with the pharmacologic drug lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase at concentrations ranging from 10(-5)-10(-8) M. After 48 hr, treatment with 10(-5)M lovastatin inhibited [3H]thymidine incorporation 55%. Flow cytometric analysis indicated that the fraction of B cells in S phase was reduced from 26.7% +/- 5.44% to 11.6% +/- 2.9% when cells were incubated with 10(-5)M lovastatin. In addition, a large peak appeared to the left of the G1 peak that was indicative of apoptosis in cells treated with 10(-5)M lovastatin. At 96 hr, the number of plaque-forming B cells was decreased 50% in the presence of lovastatin. Together these results suggest that high concentrations of lovastatin can inhibit B cell proliferation and differentiation of murine B lymphocytes in lipopolysaccharide-activated B cells, perhaps through induction of programmed cell death.

Animals↗

PubMed1995

Nitric oxide production by Sertoli cells in response to cytokines and lipopolysaccharide.

Nitric oxide (NO) is formed from L-arginine residues by nitric oxide synthase (NO Synthase) in many types of cells and acts as an intercellular messenger in several physiological systems. In the present study, we demonstrate that a combination (CL) of interleukin-1 alpha, interferon gamma, tumor necrosis factor alpha and lipopolysaccharide induces nitrite (NO2) production in cultured rat Sertoli cells. This biosynthesis of NO2- requires a lag time period of 18 hr and then increases for at least 96 hr; it is prevented by two NO Synthase inhibitors, NG-monomethyl-L-arginine and aminoguanidine. Northern blot analysis shows the induction of a macrophage-like NO Synthase mRNA synthesis in Sertoli cells cultured for a minimum of 6 hr in the presence of CL, with maximal levels after 12 to 30 hr of incubation. These results indicate for the first time that cultured rat Sertoli cells express an inducible NO Synthase isoform in response to a combination of cytokines and lipopolysaccharide.

Amino Acid Oxidoreductases↗

PubMed1997

Identification and characterization of a novel monocyte/macrophage differentiation-dependent gene that is responsive to lipopolysaccharide, ceramide, and lysophosphatidylcholine.

A novel differentiation-dependent cDNA (DIF-2) has been isolated from human mononuclear phagocytes by differential display. The full-length cDNA was cloned and sequenced. DIF-2 consists of 156 amino acids and has a predicted isoelectric point of 8.84. The mRNA is expressed in freshly isolated monocytes and is downregulated significantly when monocytes are subjected to differentiation. A similar differentiation-dependent downregulation is observed in normal hepatocytes compared to undifferentiated HepG2 cells. The mRNA expression in monocytes is sensitive to lipopolysaccharide and ceramide which both strongly increase DIF-2 transcription, while lysophosphatidylcholine results in a weaker upregulation of DIF-2 expression. A DIF-2 homologous gene has been previously isolated from mouse fibroblasts and was shown to be a serum growth factor-inducible immediate early gene. Our results indicate that DIF-2 represents a gene which is regulated in differentiation processes and strongly responsive to lipopolysaccharide, ceramide and lysophosphatidylcholine.

Amino Acid Sequence↗

PubMed1997

Nitric oxide is not involved in lipopolysaccharide and cytokine mixture-induced cellular injuries in primary cultured hepatocytes.

Nitric oxide (NO) from artificial NO donors induces cell death through complete inhibition of mitochondrial respiration of hepatocytes. Treatment of hepatocytes with lipopolysaccharide (LPS) and cytokine mixture (interferon gamma and tumor necrosis factor alpha) not only results in NO production but also causes cellular respiration suppression and cell death in hepatocytes. NG-monomethyl-L-arginine, a specific inhibitor of nitric oxide synthase, inhibits hepatocyte NO synthesis but cannot prevent hepatocytes from LPS and cytokine mixture-induced cellular injuries. Similarly, some metabolic intermediates capable of inhibiting hepatocyte NO synthesis cannot block LPS and cytokine mixture-mediated cellular injuries in hepatocytes. These results imply that lipopolysaccharide and cytokine mixture-induced cellular injuries and NO syntheses are parallel events, NO is not involved in LPS and cytokine mixture-induced cell damage.

Animals↗

PubMed1999

Interferon-gamma, bacterial lipopolysaccharide, and tumor necrosis factor-alpha induce CD11a mRNA and protein via Na+/H+ exchange and protein kinase C-dependent mechanisms in tissue macrophages.

Previously CD11a or leukocyte function-associated antigen alpha-1 was found to be induced at the surface protein level in thioglycolate-elicited peritoneal macrophages by bacterial lipopolysaccharide and interferon-gamma. To investigate this induction further, Northern blotting and enzyme-linked immunosorbent assays were used to examine the role of second messengers in CD11a gene product induction by these agents. Here I report that CD11a RNA and cell surface protein induced by bacterial lipopolysaccharide and tumor necrosis factor-alpha are sensitive to inhibition of protein kinase C, while insensitive to inhibition of Na+/H+ exchange. CD11a induction by interferon-gamma conversely is sensitive to inhibition of Na+/H+ exchange and insensitive to inhibition of protein kinase C. These observations indicate that CD11a may be induced by multiple and separate second messenger systems in primary macrophages.

Amiloride↗

PubMed1999

Involvement of endothelin-1 in up-regulation of gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide.

In this study, we investigated gastric mucosal inflammatory responses during Helicobacter pylori lipopolysaccharide-induced gastritis by analyzing the interplay between mucosal expression of endothelin-1 (ET-1), interleukin-4 (IL-4) and tumor necrosis factor-alpha (TNF-alpha). The assays conducted 4 days after intragastric dose of H. pylori lipopolysaccharide demonstrated a pattern of acute mucosal reaction characterized by the inflammatory infiltration of the lamina propria, hyperemia, and epithelial hemorrhage. This was accompanied by a 3.1-fold increase in the mucosal expression of ET-1 and a 9-fold enhancement in TNF-alpha, while the level of IL-4 showed a 20.8% decline. The results implicate ET-1 in gastric mucosal responses to H. pylori, and suggest that an increase in its level, combined with a loss of compensatory action by IL-4, may be responsible for the induction of TNF-alpha and triggering apoptotic events that exacerbate the inflammatory process.

Animals↗

PubMed1997

Similar organization of the lipopolysaccharide-binding protein (LBP) and phospholipid transfer protein (PLTP) genes suggests a common gene family of lipid-binding proteins.

The transfer of lipids in aqueous environments such as serum has been attributed to a recently characterized class of proteins. Abnormal regulation of serum lipids by these proteins is thought to be a key event in the pathophysiology of cardiovascular diseases. Lipopolysaccharide (endotoxin) binding protein (LBP) was identified by virtue of its ability to bind bacterial lipid A. We have analyzed the exon-intron organization of the LBP gene and the nucleotide sequence of its approximately 20 kb spanning 5'- and 3'-untranslated regions. When comparing the genomic organization of LBP with that of two other genes coding for lipid transfer proteins, significant homologies were found. The LBP gene includes 15 exons, and the 2-kb promoter contains recognition elements of acute phase-typical reactants and a repetitive 12-mer motif with an as yet unknown protein-binding property. Detailed sequence comparison revealed a closer relatedness of LBP with PLTP than with CETP as demonstrated by an almost identical intron positioning. This high degree of similarity supports functional studies by others suggesting that like LBP, PLTP may also be able to bind and transport bacterial lipopolysaccharide.

Acute-Phase Proteins↗

PubMed1993

Lipopolysaccharide detoxification by endotoxin neutralizing protein.

Endotoxin neutralizing protein (ENP), a recombinant form of the anti-lipopolysaccharide factor that was isolated from amebocytes of the American horseshoe crab, Limulus polyphemus, detoxifies lipopolysaccharide (LPS) both in vitro and in vivo. Using the Limulus amebocyte lysate assay, LPS was detoxified by ENP at a 1 to 1 weight ratio (1:1). When isolated rat aortic rings were preincubated for 16 hr with either LPS or LPS/ENP (1:5), only aortas in the LPS/ENP group contracted normally under norepinephrine stimulation. To show that detoxification of a lethal amount of LPS (18 mg/kg, LD50 at 48 hr) persists in vivo, LPS/albumin (1:1) or LPS/ENP (1:1) mixtures were preincubated (30 min, 37 degrees C) and then injected intravenously into rats. In the 8 hr after injection, LPS/ENP challenged rats, in contrast to their LPS/albumin injected counterparts, had significantly fewer physical signs of acute LPS toxicity (P < 0.001). At 48 hr after challenge, all LPS/ENP treated rats survived (P < 0.01 vs LPS/albumin), and with significantly less weight loss (P < 0.001 vs LPS/albumin challenged survivors). At necropsy, the LPS/ENP group was free of typical LPS-induced gross organ lesions, notably in the liver, spleen, gut-associated lymphoid tissue (GALT), and small intestine. By microscopic examination, lymphocytic necrosis in the spleen and GALT of the LPS/ENP treated survivors was significantly milder than that in the LPS/albumin challenged survivors, although the degree of hepatocellular necrosis and small intestinal enteritis was similar. LPS-neutralizing proteins such as ENP may be useful in treating LPS toxicity.

Amino Acid Sequence↗

PubMed2002

Monoclonal antibodies against Yersinia pestis lipopolysaccharide detect bacteria cultured at 28 degrees C or 37 degrees C.

Four monoclonal antibodies were generated against Yersinia pestis lipopolysaccharide by immunising mice with a cell surface preparation from Y. pestis strain 1255. In an ELISA the monoclonal antibodies reacted with live whole cells of Y. pestis strain GB cultured at 28 degrees C or 37 degrees C. The lowest detection threshold for Y. pestis strain GB cultured at 28 degrees C was 4 x 10(5) cfu ml(-1) and for bacteria cultured at 37 degrees C was 1 x 10(4) cfu ml(-1). The monoclonal antibodies did not cross react with other pathogenic Yersinia in an ELISA, but showed some cross reactivity in an immuno-blot. The monoclonal antibodies could be used for the detection of Y. pestis cultured at different temperatures and with varying plasmid profiles as the lipopolysaccharide molecule is not temperature regulated and the genes encoding its biosynthesis are located on the bacterial chromosome.

Animals↗

PubMed1993

The role of the O-antigen lipopolysaccharide on the colonization in vivo of the germfree chicken gut by Klebsiella pneumoniae.

We isolated lipopolysaccharide and capsular polysaccharide (K antigen)-defective mutants from two Klebsiella pneumoniae parental strains, and compared their ability to colonize in vivo the germfree chicken gut. The high-molecular weight lipopolysaccharide (LPS) (O antigen) was found necessary for the colonization while the capsular polysaccharide (K2 or K29) was not of importance.

Animals↗

PubMed1988

Chemical and immunochemical studies on lipopolysaccharides of Coxiella burnetii phase I and phase II.

Lipopolysaccharides of Coxiella burnetii phase I and II were comparatively investigated by chemical and immunochemical methods. LPS of phase I (LPS I) and phase II cells (LPS II) show no serological cross reaction, indicating that the serological determinants of LPS II are masked in LPS I. Chemical analysis of LPS I and II show that phase I and II cells can be considered as S and R forms of Coxiella burnetii. The structure of LPS II has recently been elucidated and shows a dimannosylated core of an alpha(1,3)-linked heptose-disaccharide which is attached to a "KDO-like" substance. In enterobacterial core-types, alpha(1,3)-linked heptose-disaccharide is also part of the inner core structure, although the heptose occurring in enterobacterial R cores is the L-glycero-D-manno-heptose. In Coxiella burnetii we have only the rare D-glycero-D-manno-heptose which is the biosynthetic precursor of the former and is in many enteric LPS, present only in addition to L-glycero-D-mannoheptose. In these R-cores, it is occupying mostly terminal positions (Radziejewska-Lebrecht et al., 1981) and is absent from the main chain. The complete structure of LPS I is not yet available, but some important points could recently be clarified. The immunodominant sugars in LPS I are C-3-branched sugars, 6-deoxy-3-C-methyl-L-gulose (L-virenose) and 3-C-(hydroxymethyl)-L-lyxose (dihydro-hydroxy-L-streptose). These two sugars have not been found so far in other lipopolysaccharides and the latter one not previously in any other natural product. Their identification is based on GLC-MS comparison with authentic and synthetic compounds. Both branched sugars (and in addition part of the mannose) are the terminal sugars in LPS I. Sites of attachment of phase I-specific sugars to the LPS II-core are: the 3-position of a branched heptose and, presumably, the 4-position of a terminal D-mannose. The extreme acid-lability of the linkages of both branched sugars was investigated in detail and is caused by the nature of the branched sugars (deoxyhexose with bulky axial substituents; pentofuranose with axial OH-groups). No information is so far available on the (penultimate) sugars to which the branched sugars are linked, but methylation analyses with LPS I, and with the recently described I/CR mutant, which is selectively lacking the virenopyranose, are presently performed.

Carbohydrate Conformation↗

PubMed1989

Production of cytokines after lipopolysaccharide stimulation of murine spleen cells during lymphoma development in AKR mice.

Injection of syngeneic lymphoma cells in AKR mice, resulted in an important increase of splenic natural killer (NK) activity in the early days following the graft. Modifications of the production of different types of cytokine: interferon, interleukins 1 and 2, tumor necrosis factor (IFN, IL-1, IL-2, TNF), involved in the regulation of NK activity, were investigated in short-term cultures of total, adherent and non-adherent fractionated spleen cells, using lipopolysaccharide as the triggering or amplifying agent. Upon stimulation with lipopolysaccharide, splenocytes from lymphoma-grafted mice released a large amount of interferon as compared to controls with a maximum level 1 day after the graft. Equal amounts of IFN-gamma and IFN-alpha/beta were detected. Treatment of spleen cells prior to culture with anti-(asialo-GM1) or anti-(Thy-1.1) antibodies reduced interferon production by 80% and 50% respectively. This finding indicates that (a) the IFN-gamma is produced by Thy-1-positive cells and (b) the production of IFN-gamma by these cells is at least partially under the control of asialo-GM1-positive cells. We also showed that non-adherent fractionated spleen cells from lymphoma-grafted mice produced IL-1 and IL-2. IL-1 was released by asialo-GM1-positive cells and IL-2 by Thy-1-positive cells. Adherent cells released only IL-1. In contrast, total cells released smaller amounts of IL-1 and IL-2, suggesting a reciprocal inhibition between subpopulations of non-adherent and adherent cells. A high level of TNF production by adherent cells was observed only 4 days after the graft. These results indicate that graft of lymphoma cells entails important modifications of spleen cell populations releasing different types of cytokines implicated in NK activation.

Animals↗

PubMed1987

Immunochemical and partial chemical characterization of fractions of membrane-bound smooth lipopolysaccharide-protein complex from Brucella abortus.

Smooth lipopolysaccharide (sLPS) of Brucella abortus was prepared and fractionated by a modification of the procedures of Moreno et al. (J. Bac. 138:361-369, 1979). Washed B. abortus cells were disrupted by 21 freeze-quick thaw cycles with ultrasonication to separate the non-membrane-bound material. Ultrasonicated bacteria were used for preparation of membrane-bound sLPS (approximately f5, the main crude sLPS fraction described by Moreno et al.). Phenol extraction was repeated 3 times and then washed with H2O 10 times to remove most of the chromogen, polysaccharides and nucleic acids, eliminating the need for enzyme treatment as described previously. The membrane-bound sLPS was fractionated into 3 to 5 groups according to the extent of dialysis and centrifugation, these fractions required only 80 ng for positive ELISA, about 0.2 ng for positive Limulus lysate tests, and reacted well with precipitating antibodies in the serum from a strain 2308 infected cow. They had marked differences in precipitin curves and chemical composition. The protein content varied from 16% to 42% as determined by dye binding test and 17 to 60% by Lowry phenol method using bovine serum albumin as the standard, which implies that the proteins associated with LPS may also play important roles in the complex for the immunochemical interactions and the heterogeneity of B. abortus lipopolysaccharide protein complex. As compared with previous reports, a higher yield of sLPS, ranging from 3.6% to 7.7% of dried bacteria, was obtained. Group f5A, which had a standard bell shaped curve in the precipitin assay, is one of the major fractions in all three strains (1119.3, 19 and 2308). The amount of other subfractions obtained varied with batches or strains of B. abortus. These results provide a new profile of the immunochemical reactivities and the heterogeneity on B. abortus smooth membrane-bound endotoxins.

Antigen-Antibody Complex↗

PubMed1989

Chemical composition of a lipopolysaccharide from Legionella pneumophila.

Lipopolysaccharide isolated from Legionella pneumophila (Phil. 1) was examined for chemical composition. The polysaccharide split off by mild acid hydrolysis contained rhamnose, mannose, glucose, quinovosamine, glucosamine and 2-keto-3-deoxyoctonate, in molar proportions 1.6:1.8:1.0:1.5:4.1:2.7. Heptoses were absent and glucose was probably mainly phosphorylated. The carbohydrate backbone of the lipid A part consisted of glucosamine, quinovosamine and glycerol, in the molar ratios 3.9:1.0:3.4, with glycerol as a phosphorylated moiety. A complex fatty acid substitution pattern comprising eight O-ester-linked, exclusively nonhydroxylated acids, and nineteen amide-linked, exclusively 3-hydroxylated acids was revealed. Both straight- and branched (iso and anteiso) carbon chains occurred. The major hydroxy fatty acid was 3-hydroxy-12-methyltridecanoic acid and six others were of a chain-length above 20 carbon atoms, with 3-hydroxy-20-methyldocosanoic acid as the longest. Two dihydroxy fatty acids, 2,3-dihydroxy-12-methyltridecanoic and 2,3-dihydroxytetradecanoic acids, were also detected. These results suggest that L. pneumophila contains a rather complex and unusual lipopolysaccharide structure of considerable biological and chemotaxonomic interest.

Carbohydrates↗

PubMed1996

Biochemical characterization of lipopolysaccharides extracted from a hydrophobic strain of Pasteurella multocida.

Lipopolysaccharides were extracted from freeze-dried cells of Pasteurella multocida strain P-1581 (serotype 8) by the phenol-chloroform-petroleum ether method and biochemically analysed using standard procedures. The primary neutral sugars were glucose, galactose and heptose. No deoxy sugars were detected. Amino sugars included galactosamine, glucosamine and glucosamine-6-phosphate. 3-Deoxy-D-manno-2-octulosonic acid was present at a relatively low concentration. The analyses included identification and quantification of phosphate and alanine. The primary fatty acids and their approximate relative ratios were 3-hydroxytetradecanoate and tetradecanoate 2:1. Tetradecanoic acid was bound almost exclusively by ester linkages. 3-Hydroxytetradecanoic acid was bound primarily by amide linkages, although significant numbers of ester-bound residues were noted. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis analyses indicated that the lipopolysaccharides were of low molecular weight.

Amino Sugars↗

PubMed1986

Lipopolysaccharide of Providencia rettgeri. Chemical studies and taxonomical implications.

The chemical constitutional analysis of the lipopolysaccharide (LPS) isolated from Providencia rettgeri was carried out. Polyacrylamide gel electrophoresis using sodium dodecylsulfate or sodium deoxycholate showed that the lipopolysaccharide mostly consisted of short sugar chains. The lipid A was precipitated out after mild acid hydrolysis of LPS. From the supernatant degraded polysaccharide and unsubstituted core fractions were isolated. Compositional analysis of the core material revealed the presence of galacturonic acid, galactose, glucose, glucosamine, L-glycero-D-manno-heptose, 3-deoxy-D-manno-octulosonic acid, alanine and phosphorus. Methylation analysis of the core material indicated the presence of terminal units of glucose, galacturonic acid and glucosamine. The chemical structure of the lipid A was elucidated. It constitutes a beta-1,6-glucosamine disaccharide substituted on either side by ester and glycosidically-bond phosphate residues. The ester-bound phosphate was found to be substituted by a 4-amino-4-deoxy-L-arabinosyl residue. The amino groups of the backbone disaccharide are N-acylated by 3-O-(14:0)14:0 and 3-O-14:0. Two hydroxyl groups of the disaccharide are esterified by 3-O-(14:0)14:0 and 3-O-14:0. The taxonomical importance of these structural details will be discussed.

Amino Sugars↗

PubMed1991

Lipopolysaccharide is the receptor for kappa phage in Serratia marcescens.

Kappa phage active on Serratia marcescens can form plaques on white and red strains with identical efficiencies. To identify the kappa phage receptor, the inactivation of the phage was studied after incubation with several bacterial subcellular fractions. The experiments demonstrated that kappa phage adsorbs to outer membrane fractions of susceptible cells. Proteinase K did not affect the rate of inactivation. Lipopolysaccharide proved to be the primary receptor for kappa phage. Prodigiosin content of the lipopolysaccharide fraction was low.

Adsorption↗