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)

The effect of adding 500 micrograms of (2,6-0-dimethyl) beta-cyclodextrin (Me-beta-CD) per ml of Stainer-Scholte (SS) medium in two-day shaker flask cultures of Bordetella pertussis on the production of lipopolysaccharide (LPS) was investigated. The amount of LPS per 10(9) cells found in the supernatants of these cultures was either somewhat reduced or unaffected by comparison with the amounts in cultures grown in SS-medium alone. In addition, the time course of LPS release from cultures of B. pertussis strain 3843 cells during a 96-h growth period in normal and Me-beta-CD-enriched SS medium is described. By using the enriched medium bacterial growth, the production of filamentous haemagglutinin (FHA) and of pertussis toxin (Pt) and the levels of haemagglutination and lymphocytosis-promoting activity were enhanced to various degrees. Measurements made on sedimented whole and on sonicated B. pertussis cells grown in the two media showed no differences in LPS content. The reasons for the reduced/unaffected LPS production are discussed. It has been suggested that an interaction between hydrophobic cavities of the Me-beta-CD molecules and the 'lipid A' part of LPS reduces the reactivity of LPS in the Limulus Amoebocyte Lysate (LAL) assay. This possibility, however, was rejected as the reactivity of Me-beta-CD-spiked purified B. pertussis strain 3803 LPS, compared with unspiked samples, remained unchanged.
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PMID:The effect of cyclodextrin on lipopolysaccharide production in cultures of Bordetella pertussis. 255 82

Human adherent monocytes stimulated with 1 microgram/ml pertussis toxin (PT) produced interleukin-1 (IL-1), as measured by thymocyte co-stimulation assay and enzyme-linked immunosorbent assay (ELISA), specific for IL-1 alpha and IL-1 beta. To clarify the role of protein kinase C (PKC) and calmodulin in IL-1 production, we investigated the effects of a PKC inhibitor, H-7, and a calmodulin antagonist, W-7 on PT- and lipopolysaccharide (LPS)-induced IL-1 production by monocytes. Addition of 10 microM and 20 microM H-7 to the culture medium markedly suppressed both PT- and LPS-induced IL-1 production. PT-induced IL-1 production was significantly suppressed by 5 microM and 10 microM W-7. However, LPS-induced IL-1 production was not suppressed by W-7 at the concentrations tested. When monocytes were labelled with Quin 2/AM, IL-1 production by monocytes stimulated with PT and LPS was markedly suppressed. These results indicate that different pathways are involved in the IL-1 production by PT and LPS; both calmodulin- and PKC-dependent processes are necessary for the IL-1 production induced by PT, whereas LPS-induced IL-1 production is dependent on the PKC. Inhibition of IL-1 production by interfering with intracellular Ca2+ trafficking in Quin 2/AM-loaded monocytes may be associated with the inhibition of PKC and calmodulin activity.
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PMID:Effect of protein kinase C inhibitor (H-7) and calmodulin antagonist (W-7) on pertussis toxin-induced IL-1 production by human adherent monocytes. Comparison with lipopolysaccharide as a stimulator of IL-1 production. 278 78

We have studied the role of cyclic adenosine 3':5' monophosphate (cAMP) in the regulation of lipopolysaccharide (LPS)-induced tumour necrosis factor (TNF) production by mouse peritoneal macrophages. LPS did not alter the intracellular levels of cAMP. However, prostaglandin E2 (PGE2) and cholera toxin, both of which are known to increase intracellular levels of cAMP, consistently inhibited LPS-induced TNF production. The cAMP analogues, dibutyryl cAMP (DbcAMP) and 8-bromo cAMP (8BrcAMP), also inhibited TNF production, whereas pertussis toxin, which inactivates the inhibitory guanine nucleotide-binding protein (Gi), had no effect. These observations suggested that LPS did not itself modify macrophage adenylate cyclase activity, while agents that increased intracellular cAMP levels were able to inhibit LPS-induced macrophage TNF production.
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PMID:Regulation of tumour necrosis factor production by mouse peritoneal macrophages: the role of cellular cyclic AMP. 284 58

The injection of killed whole-cell pertussis vaccine (PV), prepared from formulated Bordetella pertussis strains 5574 and 305, into mice was shown to produce a stimulating effect on hematopoiesis. This effect was manifested by an increase in the number of endogenic colonies developing in the spleen of mice on days 5 and 9 after their irradiation in a sublethal dose, by the sharp stimulation of the proliferative activity of splenic colony-forming units (CFUs) originating in the bone marrow and by the elevated CFUs level in the peripheral blood. The preliminary incubation of whole-cell PV with polymyxin B, cationic polypeptide selectively reacting with the lipid A moiety of lipopolysaccharide (LPS), led to a sharp decrease in the above-mentioned manifestations of hematopoietic effect of the vaccine, while incubation with cetavlon interacting with the polysaccharide moiety of LPS produced practically no effect on the capacity of the vaccine for stimulating hematopoiesis. The stimulating effect of whole-cell PV on hematopoiesis is supposedly due, to a great extent, to the lipid A moiety of LPS.
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PMID:[Polymyxin B suppresses the stimulating action of pertussis vaccine on hematopoiesis in mice]. 285 Dec 46

Antibodies to lipid A were raised in mice immunized with non-hydrolysed Bordetella pertussis microorganisms, coated with lipid A isolated from the same bacteria. Anti-lipid A activity of immune sera was measured by radioimmunoassay. Four hybrid cell lines that secrete antibodies directed against the hydrophobic region of B. pertussis lipopolysaccharide were produced by cell fusion between myeloma cells and spleen cells from immunized C3H/He-PAS mice. Differences were observed in the potency of the isolated monoclonal antibodies to inhibit B cell proliferation induced by lipopolysaccharide (LPS) or by lipid A, suggesting a selective recognition of effector sites present on the hydrophobic region of LPS.
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PMID:Inhibition of lipopolysaccharide mitogenicity with characterized anti-lipid A monoclonal antibodies. 286 28

The outer membrane (OM) component(s) from Bordetella pertussis which potentiated the antigenicity of purified Haemophilus influenzae type b capsular polysaccharide, polyribosyl ribitol phosphate (PRP), has been isolated and partially characterized. The OM was isolated from spheroplasting medium by precipitating at pH 5.0; fractionation was carried out by dissolving the crude OM in Triton X-100 followed by selective precipitation of OM in 50% ethanol. Further purification of OM was accomplished by DEAE-Sepharose 6BCL and Sephacryl S-300 chromatography. The biochemical composition and protein profiles on sodium dodecyl sulfate-polyacrylamide gel electrophoresis of various OM preparations have been examined. Combined vaccines consisting of OM components and PRP were given to young Sprague-Dawley rats, and the serum antibody to PRP was measured by an [3H]PRP binding assay. The purified OM containing mainly a 30,000-dalton protein, but not purified lipopolysaccharide or leukocytosis-promoting toxin, exhibited strong enhancement of PRP immunogenicity.
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PMID:Isolation of the outer membrane components of Bordetella pertussis which enhance the immunogenicity of Haemophilus influenzae type b capsular polysaccharide polyribosyl ribitol phosphate. 286 92

The effects of highly purified preparations of three Bordetella pertussis components--pertussis toxin (PT), lipopolysaccharide (LPS) and filamentous haemagglutinin (FHA)--were examined in the mouse weight gain test, a toxicity test for pertussis vaccine. When these components were administered alone, PT enhanced initial weight gains of the mice, LPS produced an initial weight loss and FHA had no detectable effect on the weights of the mice. However, testing the components in combinations revealed that the effect of PT and LPS together was not simply the sum of their individual effects. This combination generally produced lower weights than LPS alone, particularly in the later stages of the test.
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PMID:The effects of purified components of Bordetella pertussis in the weight gain test for the toxicity testing of pertussis vaccines. 287 67

Endotoxin protein represents a group of immunobiologically active p polypeptides which are associated with the lipopolysaccharide endotoxin in the outer membrane of Gram-negative bacteria. To study the adjuvant effect of endotoxin protein, CF-1 mice were immunized intraperitoneally with graded doses of glutaraldehyde-inactivated cholera toxoid with and without endotoxin protein prepared from Bordetella pertussis, Salmonella typhi or Vibrio cholerae. Immune responsiveness was assessed by measuring resistance to intravenous challenge with cholera enterotoxin and by serum antitoxin responses. The results showed that endotoxin protein from S. typhi can enhance the 50% protective dose (PD50) of cholera toxoid five to 12-fold, the endotoxin protein from V. cholerae enhances the PD50 six to seven fold at most, but the endotoxin protein from B. pertussis can enhance the PD50 some 27-fold. Furthermore, within the variability of both the mouse protection test and the rabbit intracutaneous assay of toxin induced vascular permeability, mouse serum neutralizing antitoxin levels correlated with the greater degree of resistance of the mice to the toxin challenge. The adjuvant effect also has been demonstrated by measuring the appearance of antitoxin specific plaque forming cells derived from mouse lymphocyte cultures. After seven days of culture in the presence of endotoxin protein and cholera toxoid, the number of plaque forming cells to cholera toxin coated sheep erythrocytes was enhanced some 28 times as compared to the cultures exposed to the cholera toxoid alone.
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PMID:The adjuvant effect of pertussis endotoxin protein in modulating the immune response to cholera toxoid in mice. 287 8

Treatment of mice by intraperitoneal inoculation of pertussis vaccine or lipopolysaccharide extracted from B. pertussis will effect resistance to rabies virus, encephalomyocarditis virus, Semliki Forest virus, and Herpes simplex virus. Our previous observations indicated that treatment of C3H/HeN (+/nu) and BDF1 mice with pertussis vaccine injected i.p. five days prior to a mouse adenovirus lethal dose i.p. challenge elicited resistance to clinical disease and death. Susceptibility returned to a portion of the test population 35 days after pertussis vaccine treatment. The pertussis vaccine induced resistance developed in athymic (nude) mice also; however, the population succumbed to infection 35 days later. Titration of pertussis vaccine with respect to induction of resistance indicated the median effective dose (ED50) was approximately 25 micrograms dry weight. This report describes the antiviral activity of acellular components extracted from pertussis vaccine. Extraction of B. pertussis cells with 1.0M NaCl and ammonium sulfate fractionation (20-40% saturation) of the extract resulted in an acellular preparation that induced resistance to lethal dose mouse adenovirus infection. The resistance inducing activity was retained after treatment of the extract with detergent (GAF Emulphogene BC 720) to remove lipopolysaccharide and adsorption to alum gel. Comparison of endotoxin content of pertussis vaccine acellular fractions, polysaccharide fraction and purified lipopolysaccharide suggested that endotoxin probably plays a role in the induction of resistance. The endotoxin content of a Emulphogene-treated preparation that protected 80% of a test population was 39 ng. The lipopolysaccharide extracted from Escherichia coli, Vibrio cholerae, Salmonella typhimurium, and Salmonella minnesota did not induce a resistant state seven days after administration; however, lipopolysaccharide extracted from B. pertussis induced a resistant state.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunomodulation by Bordetella pertussis: antiviral effects. 287 9

The serum antibody responses of vaccinated children and whooping cough patients to the highly purified Bordetella pertussis antigens, leukocytosis-promoting factor (LPF), lipopolysaccharide (LPS), a protein binding to complement-fixing antibodies induced during whooping cough (PBCA) and to a partly purified filamentous hemagglutinin fraction (FHA) were analysed in enzyme-linked immunosorbent assay. Of the IgG antibodies, those to FHA and LPS were often persistent both after infection and vaccination. The mean titers were about six to ten times higher after disease than after vaccination in corresponding age groups. IgG antibodies to LPF were frequently detected in high titers in patients (mean arbitrary units = 1723), but seldom in low titers (mean units = 20), after vaccination. IgG antibodies to PBCA disappeared some years after vaccination. IgM antibodies to PBCA, FHA and LPS were present in almost 100% after vaccination and disease. IgM antibodies to LPF were detected in 23% of the vaccinated and in 83% of the patients. The respective mean IgM units to PBCA, FHA, LPS and LPF were 14, 13, 16 and 134 times higher in patients than in vaccinated children. None of the vaccinated children and 20% of the patients had IgA antibodies to LPF. No pronounced differences in the percentage of the respective IgA responses to PBCA, the FHA fraction and LPS were found between the two groups. The striking differences in the immune response of vaccinated children and patients were to LPF. Since whooping cough protects better than vaccination against B. pertussis infection, the present study indicates that immunogenic LPF should be included in an acellular vaccine. Also addition of FHA, PBCA and possibly even of LPS, if it can be prepared in an immunogenic and atoxic form, might be necessary in order to prepare a highly effective acellular vaccine.
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PMID:Antibody responses after vaccination and disease against leukocytosis promoting factor, filamentous hemagglutinin, lipopolysaccharide and a protein binding to complement-fixing antibodies induced during whooping cough. 287 24


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