Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The roles of carrier and adjuvant in the induction of primary antibody responses to the haptenic drug chlorhexidine (which interacts only electrostatically with proteins) and its N-chlorinated derivative (which binds covalently to proteins) were investigated. N-chloro chlorhexidine, covalently linked to either ovalbumin, KLH, thaumatin, LPS-associated protein or human serum protein, but not autologous mouse serum protein or LPS itself, induced both IgE and IgG anti-chlorhexidine antibody synthesis when injected, with alum adjuvant, into BALB/c mice. Bordetella pertussis (BP) could function as both carrier and adjuvant, but no response was obtained by injection of N-chloro chlorhexidine alone or with alum adjuvant. The immunogenicity of N-chlorinated chlorhexidine was directly related to the degree of its substitution onto the carrier which, in turn, was proportional to the level of chlorine (mM) employed. Chlorine also affected the immunogenicity of the various carriers. In the absence of chlorine, chlorhexidine induced only low level IgG antibody synthesis, but only if presented in a 'pseudoplurivalent' form, as a chlorhexidine-mediated protein precipitate (with alum) or electrostatically bound to a particulate carrier such as BP.
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PMID:Factors influencing the immunogenicity of the haptenic drug chlorhexidine in mice. II. The role of the carrier and adjuvants in the induction of IgE and IgG anti-hapten responses. 379 38

Pertussis vaccine consisting of inactivated whole Bordetella pertussis organisms appears to induce a biphasic response on the glucose metabolism of N:NIH mice. A heat stable component assumed to be the LPS induces a transient hyperglycaemia within 6 hours after vaccination. A heat labile component assumed to be LPF, induces a hypoglycaemia and hyperinsulinaemia 2-7 days after treatment. A purified vaccine examined in this study still showed some effects on the glucose metabolism at 3-4 days after vaccination. If hypoglycaemia contributes to the neurological side effects, incidentally observed after vaccination of infants, both LPS and LPF have to be considered to be responsible for these effects.
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PMID:A biphasic glucose and insulin response in mice after vaccination with pertussis vaccine. 390 Oct 31

Endotoxin prepared from several Bordetella pertussis strains in both immunological phases I and IV gave two lipopolysaccharide peaks (LPS-I and LPS-II) when analyzed on hydroxylapatite columns in a phosphate buffer containing 0.1% sodium dodecyl sulfate; these lipopolysaccharides, present in the ratio of 2:3, are true endotoxins by both chemical and biological criteria. Endotoxins isolated from Escherichia coli, Salmonella typhimurium, and Shigella flexneri gave single lipopolysaccharide peaks when analyzed by the same procedure. Upon hydrolysis with acetic acid (pH 3.4) at 100 degrees C for 1 h, LPS-I released a polysaccharide (PS-I); the linkage broken was that of the glycosidic bond of a non-phosphorylated 3-deoxy-oct-2-ulosonic acid. Treatment with 0.25 M mineral acid at 100 degrees C for 30 min was required to free the polysaccharide moiety (PS-II) of LPS-II, the linkage broken being the glycosidic bond of a phosphorylated 3-deoxy-oct-2-ulosonic acid. Chemical and physical differences of the polysaccharide moieties PS-I and PS-II present in LPS-I and LPS-II have been described previously (25). By using the technique of 125I labeling, it was shown that the totality of labeled proteins present in the endotoxin extracted from Bordetella pertussis by the phenol-water procedure could be separated from the lipopolysaccharide by column chromatography on hydroxylapatite; it follows that these proteins are not linked by covalent bonds to the lipopolysaccharide.
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PMID:Isolation of two protein-free and chemically different lipopolysaccharides from Bordetella pertussis phenol-extracted endotoxin. 624 93

The Bordetella pertussis endotoxin, labeled with tritium ((3H)-LPS), bound irreversibly and nonspecifically to rabbit lung macrophages, but bound reversibly and specifically to both resident and elicited rabbit peritoneal macrophages. The specific binding capacity of the macrophages was saturated with about 3 X 10(4) LPS molecules per cell. The binding was inhibited with the homologous unlabeled endotoxin, but not at all with endotoxin from Proteus mirabilis, thus assessing ligand specificity. Endotoxins from other bacteria gave intermediate inhibition value. Binding of tritium-labeled pertussis endotoxin was significantly inhibited by one of the two polysaccharides (PS-1) present in this endotoxin, but neither the other polysaccharide (PS-2) nor the Lipid A fragment exhibited such activity. These results strongly suggest the presence of a lectin-like receptor for LPS on the membrane of rabbit peritoneal macrophages.
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PMID:Lipopolysaccharide receptor on rabbit peritoneal macrophages. I. Binding characteristics. 627 22

Infections of the deeper respiratory airways can contribute to the progression of chronic asthmatic bronchitis. In the present report a number of microorganisms affecting the number of beta-adrenoceptors in guinea-pig lung homogenates are described. Haemophilus influenzae, Streptococcus pneumoniae, Bordetella pertussis and Escherichia coli O111B4 induced a significant decrease of the number of beta-adrenoceptors (by approximately 20%). Staphylococcus aureus, influenza A virus and Escherichia coli J5 were not active. These data point to a common factor shared by gram-negative bacilli; i.e. endotoxin. Purified endotoxin of E. coli O111B4 also decreased the number of beta-adrenoceptors, while E. coli J5-LPS did not. This suggests that neutral polysaccharides of bacterial cell walls, especially those in the 'O'-antigenic side chain of gram-negative endotoxins may be responsible for the decrease of beta-adrenoceptor number and therefore contribute to the pathogenesis of chronic asthmatic bronchitis. Intact endotoxin seems to be necessary since neither the isolated lipid nor the polysaccharide part of E. coli O111B4 LPS affected the number of beta-adrenoceptors in the lung.
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PMID:Bacterial cell wall components decrease the number of guinea-pig lung beta-adrenoceptors. 630 48

The effect of B. pertussis vaccine on the serum glucose level of mice was investigated. The results show that at least two components in the vaccine interfere with glucose metabolism. A heat-stable component which is assumed to be LPS induced hypoglycemia 3-5.5 h after inoculation, especially in LPS-sensitized mice. A heat-labile component which is possibly equivalent with the LPF/HSF/IAP complex, is responsible for persistence of the hypoglycaemia for at least 6 days. If hypoglycaemia contributes to the neurological side effects after pertussis vaccination both components have to be considered as being responsible for these effects.
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PMID:A biphasic serum glucose response in mice to inoculation with pertussis vaccine. 673 46

Binding of FMLP to the neutrophil N-formyl peptide receptor (FPR) transmits signals through pertussis toxin-sensitive G proteins triggering Ca2+ flux, superoxide production, granule exocytosis, and neutrophil aggregation and adhesion involving the beta 2 (CD18) integrins. Expression of the FPR in mouse fibroblasts or human kidney cells has been shown to confer an N-formyl peptide-inducible Ca2+ flux in transfectants. Here we demonstrate that the transfected receptor can also support ligand-induced alterations in cellular adhesion. We established stable transfectants of mouse L1-2 pre-B cells with cDNA for human FPR (L1-2 FPR cells). The transfectants bind N-formyl-Nle-Leu-Phe-Nle-Tyr-Lys-fluorescein with 1.4 x 10(5) sites per cell and a dissociation constant of 3.3 nM. Stimulation with FMLP induces a transient Ca2+ flux. FMLP also triggers adhesion of L1-2 FPR cells to TNF-alpha- or LPS-activated bEnd3 cells (mouse brain-derived endothelial cells) and to purified mouse VCAM-1. Binding is inhibited by Abs to VCAM-1 and to the alpha-chain of its lymphocyte receptor (the alpha 4 beta 1 integrin, VLA-4). Stimulation with FMLP does not induce a change in cell surface expression of alpha 4. Induced adhesion to VCAM-1 is rapid, detectable at the earliest times measurable (30 to 60 s after FMLP addition), and is inhibited by pertussis toxin. We conclude that FPR can mediate integrin activation not only in neutrophils but also in lymphocytes, and can trigger rapid adhesion via lymphocyte alpha 4 beta 1. The adhesion of lymphocytes is critical to their migration and targeting; our results suggest the possibility of manipulating adhesive responses through expression of chemoattractant receptors in lymphoid cells engineered for cellular therapy, allowing targeted adhesion and potentially migration in response to locally administered ligands.
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PMID:Ligand-induced adhesion to activated endothelium and to vascular cell adhesion molecule-1 in lymphocytes transfected with the N-formyl peptide receptor. 751 63

125I-ASD photoaffinity-labeling derivatives of pertussis toxin (125I-ASD-PT) or lipopolysaccharide (125I-ASD-LPS) labeled similar 70-kDa proteins in Jurkat cells, a cell line derived from human CD4+ T lymphocytes. Labeling of this 70-kDa protein by 125I-ASD-PT was inhibited by underivatized PT but not by underivatized LPS. However, an immunoglobulin M monoclonal antibody with specificity for the p73 LPS receptor in murine splenocytes (S. W. Bright, T.-Y. Chen, L. M. Flebbe, M.-G. Lei, and D. C. Morrison, J. Immunol. 145:1-7, 1990) inhibited 125I-ASD-PT labeling of the 70-kDa species in Jurkat cells. Our results suggested that PT may bind to the same 70-kDa protein as LPS does in Jurkat cells but that PT and LPS bind to different sites on this receptor candidate. 125I-ASD-PT photoaffinity labeling of the 70-kDa protein was also inhibited by underivatized glycoproteins to which PT has been shown to bind, and this inhibition correlated with the relative binding affinities of the glycoproteins for PT. 125I-ASD derivatives of two sialic acid-specific plant lectins, Maackia amurensis leukoagglutinin and Sambucus nigra agglutinin, with oligosaccharide binding specificities similar to those of PT also labeled a 70-kDa protein in Jurkat cells. This suggests that the 70-kDa PT receptor candidate in Jurkat cells likely contains sialooligosaccharide sequences to which PT, M. amurensis leukoagglutinin, and S. nigra agglutinin bind. The cross-reacting epitope recognized by monoclonal antibody 5D3 in this 70-kDa species might overlap the PT- and LPS-binding sites.
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PMID:The 70-kilodalton pertussis toxin-binding protein in Jurkat cells. 751 75

Pertussis toxin (Ptx) is a hexameric protein with classical AB architecture produced by Bordetella pertussis. The aim of this study was to investigate the effect of Ptx on migration of polymorphonuclear leukocytes to site of inflammation and on cell-dependent edema. Ptx was purified from the supernatant of the culture medium of B. pertussis using hydroxylapatite chromatography and fetuin affinity chromatography. Ptx induced a maximal clustering of Chinese hamster ovary cells at concentrations as low as 0.1 ng/ml. Intravenous injection of Ptx (400 ng) significantly blocked the neutrophil migration induced by 200 ng of lipopolysaccharide (LPS from E. coli O111:B4; 2.27 +/- 0.13 vs 0.61 +/- 0.16 per 10(6) neutrophils/ml; P < 0.001; N = 5) and by 200 ng of formyl-methionyl-leucyl-phenylalanine (fMLP; 2.53 +/- 0.45 vs 0.75 +/- 0.14 per 10(6) neutrophils/ml; P < 0.01; N = 6) into the peritoneal cavities of male Wistar rats (weighing 150-180 g). In addition, Ptx (400 ng) pretreatment also blocked the edema induced by intraplantar injection of 100 micrograms carrageenin (delta increase in volume: 0.667 +/- 0.087 vs 0.313 +/- 0.058 ml; P < 0.01; N = 5) but not the edema induced by 100 micrograms dextran (delta increase in volume: 0.537 +/- 0.06 vs 0.385 +/- 0.076 ml; P > 0.05; N = 5). These data demonstrate that Ptx blocked neutrophil migration induced by a direct fMLP stimulus of a site of inflammation. In addition, this toxin blocks the indirect stimulus of LPS on neutrophil migration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pertussis toxin from Bordetella pertussis blocks neutrophil migration and neutrophil-dependent edema in response to inflammation. 758 Oct 20

1. Purinoceptor agonist-induced currents in untreated (proliferating) and lipopolysaccharide- (LPS; 100 ng ml-1) treated (non-proliferating) rat microglial cells were recorded by the whole-cell patch-clamp technique. 2. In non-proliferating microglia, adenosine (0.01-100 microM), 2-methylthio ATP (3-3000 nM), ATP (0.1-1000 microM), and ATP-gamma-S (1-10 microM), but not alpha,beta-methylene ATP (alpha,beta-MeATP; 100 microM) produced a slow outward current at a holding potential of 0 mV. When K+ was replaced in the pipette solution by an equimolar concentration of Cs+ (150 mM), the 2-methylthio ATP- (300 nM) induced outward current disappeared. The effect of 2-methylthio ATP (300 nM) did not depend on the presence of extracellular Mg2+ (1 mM). The outward current response to 2-methylthio ATP (300 nM) was larger in proliferating than in non-proliferating microglia. 3. ATP (1-1000 microM) evoked a fast inward current at a holding potential of -70 mV in nonproliferating microglia, while adenosine (100-1000 microM) was inactive. When the effects of ATP were compared at 0 and -70 mV, it became evident that ATP is much more potent in evoking the outward current. 4. The 2-methylthio ATP- (300 nM) induced outward current was blocked by suramin (300 microM), but not by 8-(p-sulphophenyl)-theophylline (100 microM), while the adenosine- (1 microM) induced outward current had the reverse sensitivity to these antagonists. 5. The 2-methylthio ATP- (300 nM) induced outward current was inhibited by inclusion of GDP-beta-S(200 microM) into the pipette solution or by preincubation of microglial cells with pertussis toxin(50 ng ml-1) for 12 h. The 2-methylthio ATP- (300 microM) induced inward current was not changed by intracellular GDP-beta-S (200 microM). The outward current response to adenosine (1 microM) was also abolished after pretreatment with pertussis toxin (50 ng ml-1).6. Rat microglia possess both ATP-sensitive P2y- and adenosine-sensitive P1-purinoceptors. The ATP evoked inward current is mediated by P2y-purinoceptors, while the ATP- and adenosine-evoked outward currents are mediated by P2y- and P1-purinoceptors, respectively. The transduction mechanisms of the outward, but not the inward current activation involve a pertussis toxin-sensitive G protein.
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PMID:Characterization and transduction mechanisms of purinoceptors in activated rat microglia. 781 23


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