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)

We have isolated from Bordetella pertussis an oligopeptide with characteristic amino acid composition. This peptide was applied to mice in standardized tests for pertussis immunization. In three tests with three independent isolates of peptide, a significant and dose dependent protection was observed. One microgram of peptide per mouse produces the same protective effect as 0.1 IU of pertussis vaccine. It is important to note that similar peptides can be isolated from other bacteria and other DNA containing cellular organisms which have specific amino acid compositions and which are antigens specific for the organism from which they were isolated. The antigens are very potent, e.g., one ng of Mycobacterium tuberculosis peptide is equivalent to one unit of tuberculin. It is conceivable that immunizing effects such as those observed for pertussis are common to the peptides of this group. Since all such peptides are isolated from a group of low molecular weight ribonucleoproteins, as first reported by WILHELM, we propose the term nucleopeptides for this group. Oligopeptides of the nucleopeptide group are now available for sequence analysis. We expect that synthetic peptides of this group will become available in time for diagnosis, prophylaxis and therapy of a number of diseases.
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PMID:[Protection against infection with Bordetella pertussis by an oligopeptide from Bordetella pertussis (author's transl)]. 7 6

The lymphocytosis-promoting factor of Bordetella pertussis is a potent mitogen for murine lymphocytes in vitro. The stimulatory response was not the result of specific antigen stimulation. Spleen and lymph node cells were responsive, whereas normal thymocytes were unresponsive. However, DNA replication was induced in cortisone-resistant thymocytes by lymphocytosis-promoting factor (LPF). Bone marrow cells were not stimulated by LPF.
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PMID:The in vitro effects of Bordetella pertussis lymphocytosis-promoting factor on murine lymphocytes. I. Proliferative response. 18 15

Administration of Bordetella pertussis and some of their components to mice induced an increase of DNA-binding activity of the sera revealed under ionic strength conditions of physiological saline, mostly on the 14th day. It was shown by the inhibition method that interaction between mouse sera and native DNA was specific. Maximum increase in the quantity of mouse sera proteins reacting with DNA under low ionic strength condition of physiological saline (0.05 M NaCl) is revealed on the 7th day. However, in administration of Bordetella pertussis and their cytoplasmic membrane the elevated DNA-binding proteins content persisted up to 14 days.
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PMID:[Induction of antibodies to native DNA by components of Bordetella pertussis]. 21 Aug 65

Distinguished lymphocytes stimulation was observed in vitro with one out of four patients received Trasylol therapy. The peak response of DNA synthesis was shown to occur at 100 mug/tube of basic pancreatic trypsin inhibitor (BPTI) itself, about 6 days after addition of BPTI. Reactivity (3H-thymidine incorporation) of lymphocytes of patients after the therapy, to specific antigen, ie., purified protein derivative (PPD) or Bordetella pertussis organisms in vitro, was markedly depressed. On the other hand, that to non-specific mitogen, phytohaemagglutinin-p of pokeweed mitogen, was a little reduced, or rather enhanced after the therapy. Conversly, lymphocytes of an originally tuberculin negative patient were lead to be stimulated with PPD in vitro, after skin test with PPD and Trasylol therapy. These various immune responses including drug-induced exanthemas of patients received the therapy, are discussed in this report, in comparison with immune responses of guinea pigs sensitized with BPTI, immune responses of animals in microorganism infections and the contrary immunological effects of Trasylol already reported.
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PMID:Stimulation of lymphocytes of patients administered with a trypsin inhibitor, Trasylol (basic pancreatic trypsin inhibitor pharmaceutical), in vitro with BPTI and other several stimulants. 108 80

We have cloned and sequenced new Escherichia coli genes which belong to member of the family of environmentally responsive two-component system and named evgA and evgS because their amino acid sequences were found the most homologus to the Bordetella pertussis bvgA and bvgS. They were mapped at 51 min. and extending from 6B9 to 7G9 in the Kohara miniset library of the E. coli chromosome. In fact, both EvgA and EvgS proteins predicted from their DNA sequences were identified in the in vitro coupled transcription translation system. When the evgA and evgS were expressed on multiple copy plasmid in an envZ deletion strain, ompC expression was also regulated by temperature, MgSO4 and nicotinic acid, by which virulence of Bordetella pertussis is controlled via BvgA and BvgS. These results indicate that ompC expression was controlled by in vivo cross-talk via EvgA and EvgS which can work in E. coli the same way as BvgA and BvgS.
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PMID:Cloning and sequence analysis of the evgAS genes involved in signal transduction of Escherichia coli K-12. 128 96

Using 3T3 and 3T6 mouse fibroblasts and A431 epidermoid carcinoma cells, we previously observed that extracellular ATP and ADP were mitogens and they synergized with other growth factors (Huang, N., Wang, D. and Heppel, L. A. (1989) Proc. Natl. Acad. Sci. USA 86, 7904-7908). We now report that ATP and ADP stimulated Na+ entry, intracellular alkalinization and Na+/K+ pump activity, which are early events that had been proposed to play a central role in DNA synthesis. In addition, ATP, ADP and AMPPNP stimulated uridine uptake by a pathway involving arachidonic acid metabolism. In A431 cells, activation of protein kinase C also contributed to ATP-dependent stimulation of uridine uptake. Concentrations of indomethacin and pertussis toxin which inhibited uridine uptake also blocked arachidonic acid metabolism and DNA synthesis. ATP acted as a competence factor. Interestingly, ATP did not have to be continuously present to stimulate uridine uptake. It was equally effective even when it was washed away after brief treatment of cells.
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PMID:Extracellular ATP stimulates increases in Na+/K+ pump activity, intracellular pH and uridine uptake in cultures of mammalian cells. 131 Mar 99

The purpose of the study was to determine the physiological actions of amylin, a novel 37-amino acid peptide isolated from pancreatic islet amyloid deposits. Our results showed that an infusion of amylin reduced fasting plasma insulin levels and impaired glucose tolerance in mice. Amylin significantly reduced insulin secretion in rat insulinoma cell lines (Rin m5F cells) that were stimulated by either isoproterenol and forskolin, but it did not affect insulin secretion stimulated by isobutyl-methylxanthine (IBMX) or dibutyryl cyclic-adenosine monophosphate (db-cAMP). Amylin also reduced cAMP levels in Rin m5F cells in response to isoproterenol, but did not affect cAMP levels in cells pretreated with pertussis toxin. These results suggest that the reduction of cAMP by amylin may be mediated through pertussis toxin-sensitive Gi proteins. Amylin significantly reduced basal and insulin-stimulated glycogen synthesis in rat primary cultured hepatocytes. Amylin stimulated basal and insulin-stimulated lipogenesis in hepatocytes. Amylin did not affect DNA synthesis in hepatocytes. These results suggest that amylin conducts dispersion actions on in vivo glucose metabolism in rat, and in vitro insulin secretion from Rin m5F cells and metabolism in rat hepatocytes.
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PMID:The effects of amylin on insulin secretion from Rin m5F cells and glycogen synthesis and lipogenesis in rat primary cultured hepatocytes. 131 71

alpha-Thrombin (thrombin) stimulates phospholipase C and modulates the activity of adenylate cyclase in a number of cell types via G protein-coupled receptors. It is also a potent growth factor, notably for a line of hamster fibroblasts (CCL39 cells). Recently, predicted amino acid sequences for human and hamster thrombin receptors have been reported that display a putative thrombin cleavage site in the N-terminal extracellular domain. Synthetic peptides corresponding to 14 residues carboxyl to the presumed thrombin cleavage site of the human receptor have been shown to activate platelets as well as the thrombin receptor expressed in Xenopus oocytes. In the present study we have examined the effects of synthetic peptides corresponding to the same region of the hamster receptor (S-42-L-55) and shorter peptides (2-7 residues) on signal transducing systems in CCL39 cells. Our results indicate that hamster receptor peptides of greater than or equal to 5 residues effectively stimulate phospholipase C in CCL39 cells via the thrombin receptor and induce rapid desensitization of the response. The same peptides also inhibit adenylate cyclase in a pertussis toxin-sensitive manner. Although the peptides are potent agonists of serotonin release in platelets, unlike thrombin, by themselves they are not mitogenic. However, they potentiate DNA synthesis in cooperation with growth factors possessing tyrosine kinase receptors. Hence, we conclude that the potent mitogenic action of thrombin cannot be accounted for solely by the activation of the cloned receptor. We postulate the existence of an additional receptor activated by thrombin, which is required for its full mitogenic potential.
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PMID:Synthetic alpha-thrombin receptor peptides activate G protein-coupled signaling pathways but are unable to induce mitogenesis. 131 81

Lucifer yellow (LY) accumulation was used to measure macrophage pinocytosis. The hematopoietic growth factors, macrophage colony-stimulating factor (CSF-1), granulocyte-macrophage CSF (GM-CSF), and interleukin 3, and the macrophage activators, lipopolysaccharide and zymosan, all stimulated LY uptake in both murine bone marrow-derived macrophages (BMMs) and resident peritoneal macrophages (RPMs) without affecting LY efflux. The stimulation of pinocytosis in the poorly cycling RPMs and in BMMs by nonmitogens dissociates stimulation of pinocytosis from subsequent DNA synthesis. Regulation of pinocytosis in BMMs appears to be independent of that of urokinase-type plasminogen activator expression. The increases in CSF-mediated BMM pinocytosis were not inhibited by pertussis toxin, by elevations in intracellular cAMP, or by glucocorticoids and were only partially inhibited by inhibitors of Na+/H+ antiport and Na+/K(+)-ATPase activities. Protein kinase C activation could be involved in regulating BMM pinocytosis because phorbol myristate acetate, oleoylacyglycerol, and exogenously added phospholipase C can all stimulate it. Ca2+ ionophores were inactive, whereas the Na+/H+ ionophore monensin potently inhibited BMM pinocytosis.
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PMID:Regulation of pinocytosis in murine macrophages by colony-stimulating factors and other agents. 131 79

Agonist occupancy of the alpha 2-C10 adrenergic receptor in a stable clone (1C) of Rat 1 fibroblasts produced by transfection of cells with genomic DNA encoding this receptor causes the activation of both of the pertussis-toxin-sensitive G-proteins Gi2 and Gi3 [Milligan, Carr, Gould, Mullaney & Lavan (1991) J. Biol. Chem. 266, 6447-6455]. An IgG fraction from an antiserum (I3B) which identifies the C-terminal decapeptide of Gi3 alpha only was able to inhibit partially receptor stimulation of high-affinity GTPase activity. An equivalent fraction from an antiserum (AS7) able to identify the C-terminal decapeptide of Gi1 alpha + Gi2 alpha, but not Gi3 alpha, was also able to inhibit partially receptor stimulation of GTPase activity, and the effects of the two antisera were additive. By contrast, agonist-mediated inhibition of forskolin-amplified adenylate cyclase activity was abolished completely by the IgG fraction of antiserum AS7, but was not decreased by treatment with antiserum 13B. Based on the proportion of agonist-stimulated high-affinity GTPase which was prevented by each antiserum and on the measured membrane levels of Gi2 and Gi3, calculations indicated that essentially all of the cellular Gi3, but only 15% of the available Gi2, can be activated by the alpha 2-C10 adrenergic receptor in these cells. These results demonstrate that, although Gi3 is activated by alpha 2-adrenergic agonists in membranes of clone 1C cells, it does not contribute to the transduction of receptor-mediated inhibition of adenylate cyclase.
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PMID:Gi3 does not contribute to the inhibition of adenylate cyclase when stimulation of an alpha 2-adrenergic receptor causes activation of both Gi2 and Gi3. 131 36


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