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)

In order to analyze the role of phagocytic cells in experimental antitubular basement membrane (TBM) antibody-mediated nephritis, Hartley guinea pigs (GP) were immunized with rabbit tubular basement membrane (TBM) in complete Freund's adjuvant and pertussis vaccine. Renal tissue was obtained 10 to 15, 15 to 25, and 25 to 35 days after the start of immunization. Severe renal tubulointerstitial (RTI) nephritis developed in 95% of the animals. Linear deposits of IgG and C3 along TBM were seen 10 days after initial immunization. A few days later, monocytes and macrophages infiltrated the interstitium and subsequently differentiated into epithelioid and foreign body-type giant cells (GC). The GC were most actively involved in the destruction of the TBM: Cytoplasmic pseudopodia of the GC adhered to the TBM; the areas of membrane apposition were several microns in length; no evidence of specialization was found in the plasma membrane adjoining the TBM; no cellular organelles, except for abundant microfilaments, were seen in the contact regions. The initial contact was followed by lysis of plasma membrane of the GC and TBM, perforation of TBM, and phagocytosis of TBM fragments. Concomitantly, fluorescent staining for IgG along the TBM became discontinuous or disappeared. Destruction of TBM was accompanied by degeneration of tubular epithelial cells and collapse of tubular architecture. The morphologic observations are consistent with the hypothesis that, in GP, autoimmune RTI nephritis damage of TBM results from the cooperation of humoral and cellular mechanisms, probably akin to those of antibody-mediated lymphocytotoxicity.
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PMID:Structural observations on epithelioid and giant cells in experimental autoimmune tubulointerstitial nephritis in guinea pigs. 57 43

The effects of guanosine 5'-triphosphate (GTP) and GTP-gamma-S, known activators of GTP binding proteins, on proton transport were investigated in endosome-enriched vesicles (endosomes). Endosomes were prepared from rabbit renal cortex following the intravenous injection of FITC-dextran. The rate of intravesicular acidification was determined by measuring changes in fluorescence of FITC-dextran. Both GTP and GTP-gamma-S stimulated significantly the initial rate of proton transport. In contrast, GDP-beta-S, which does not activate GTP binding proteins, inhibited proton transport. The rank order of stimulation was GTP-gamma-S greater than GTP greater than control greater than GDP-beta-S. GTP-gamma-S stimulation of proton transport was also observed under conditions in which chloride entry was eliminated, i.e., 0 mM external chloride concentration in the presence of potassium/valinomycin voltage clamping. GTP-gamma-S did not affect proton leak in endosomes as determined by collapse of H+ ATPase-generated pH gradients. ADP ribosylation by treatment of endosomal membranes with pertussis toxin revealed two substrates corresponding to the 39-41 kD region and comigrating with alpha i subunits. Pretreatment of the membranes with pertussis toxin had no effect on proton transport in the absence of GTP or GTP-gamma-S. However, pretreatment with pertussis toxin blocked the stimulation of proton transport by GTP. In contrast, as reported in other membranes by others previously, pertussis toxin did not prevent the stimulation of proton transport by GTP-gamma-S. These findings, taken together, indicate that GTP binding proteins are present in endosomal membranes derived from renal cortex and that activation of G protein by GTP and GTP-gamma-S stimulates proton transport in a rank order identical to that reported for other transport pathways modulated by Gi proteins. Therefore, these studies suggest that G proteins are capable of stimulating the vacuolar H ATPase of endosomes directly.
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PMID:A potential role for guanine nucleotide-binding protein in the regulation of endosomal proton transport. 185 Jul 57

Propionic acid induces a calcium mobilization in human neutrophils which is prevented by pretreatment with phorbol ester or pertussis toxin. The effect is reminiscent of that of chemotactic factors and leukotriene B4 and was attributed to cytoplasmic acidification (Naccache, P.H. et al. (1988) J. Cell. Physiol. 136, 118-124). We show there that other weak acids also induced cytoplasmic alkalinization and calcium mobilization. However, addition of trimethylamine together with propionic acid prevented the cytoplasmic acidification without modifying the calcium mobilization. Propionic acid increased the production of inositol phosphates but this effect was largely prevented by the joint addition of trimethylamine. The ionophores nigericin and monensin can both be forced to produce either cytoplasmic acidification or alkalinization by manipulating the extracellular concentrations of Na+, K+ or H+. Both ionophores produced calcium mobilization in all the cases, irrespective of the direction of the cytoplasmic pH shift. The ionophores were documented to collapse existing pH gradients among the cytoplasm and intracellular compartments. We conclude that the calcium-mobilizing effect of propionic acid and other weak acids is not due to the acidification of the cytoplasm. Our results are consistent, however, with calcium mobilization induced by weak acids and ionophores arising from acidification of an alkaline intracellular compartment.
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PMID:The role of intracellular acidification in calcium mobilization in human neutrophils. 204 5

Tumour necrosis factor (TNF) is an important mediator of endotoxin-induced vascular collapse and other inflammatory reactions. Eicosanoids have been implicated in the pathogeensis of these responses. In order to explore further the potential interactions between TNF and eicosanoid metabolism in eliciting vascular responses, we studied the effects of TNF on the bovine endothelial cell line CPAE. TNF induced cellular retraction observed by light microscope. This morphological change was monitored by the passage of iodinated protein A between adjacent cells and by release of [3H]arachidonic acid metabolites from cells. Both the morphological and functional responses were abrogated by inhibition of eicosanoid synthesis with BW755c. The release of [3H]arachidonic acid metabolites appeared to be mediated by a transient increase in phospholipase A2 activity. Phospholipase C activity was not affected by TNF. The maximal increase in phospholipase A2 activity occurred at 5 min following the addition of TNF. Phospholipase A2 activation, [3H]arachidonic acid-metabolite synthesis and passage of iodinated protein A, required both RNA and protein synthesis and were associated with an increase in the synthesis of a recently described phospholipase A2-activating protein. The Bordetella pertussis toxin, islet-activating protein, also inhibited the increase in phospholipase A2 activity, the release of [3H]arachidonic acid metabolites and the passage of iodinated protein A, suggesting that the TNF receptor-ligand interaction resulting in cellular retraction, phospholipase A2 activation and eicosanoid synthesis, is coupled through the Ni guanine nucleotide regulatory protein in these cells.
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PMID:Tumour necrosis factor (cachectin) induces phospholipase A2 activity and synthesis of a phospholipase A2-activating protein in endothelial cells. 312 74

The incidence and type of reactions after administration of plain and adsorbed diphtheria-tetanus-pertussis vaccine were recorded in a blind controlled prospective study of 2041 vaccinations in 1075 infants receiving routine childhood immunization. There was no significant difference in the total incidence or type of general reactions after plain and adsorbed vaccine, but local reactions were significantly less frequent after plain vaccine. General reactions were recorded after 41.5% of vaccinations with plain vaccine and after 40.8% of vaccinations with adsorbed vaccine. Local reactions were reported in 66.7% and 76.5% of recipients respectively. The most commonly reported systemic reactions were irritability and fever. Three recipients of plain vaccine and one of adsorbed vaccine suffered hyporesponsiveness or collapse. One recipient of each vaccine suffered a convulsion. No persisting sequelae were recorded.
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PMID:The incidence and type of reactions to plain and adsorbed DTP vaccines. 389 84

An ad hoc panel of the American Medical Association prepared a report to identify severe, irreversible pertussis vaccine reactions and to establish criteria for attributing such reactions to the vaccine. Severe but reversible reactions, their likely duration and effects, and the clinical criteria for attribution were also examined. Three types of reactions which may produce residual brain damage lasting more than one year are encephalopathy, complex febrile convulsions, and afebrile convulsions. Serious pertussis vaccine reactions which are unlikely to have persistent adverse effects are simple febrile convulsions, anaphylaxis, and shock collapse. The panel also noted that there is no evidence that killed vaccine such as the pertussis vaccine can cause any insidious, delayed harmful effects.
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PMID:Pertussis vaccine injury. AMA Ad Hoc Panel on Pertussis Vaccine Injury. 405 31

Voluntary reporting of vaccine reactions was intensified in a single large region for 7 years Anaphylaxis and collapse, convulsion, and neurological disorder were reported most frequently after diphtheria/tetanus/pertussis (DTP). The greater frequency of recorded reactions after DTP than after DT could have been due to bias caused by the adverse publicity accorded to pertussis vaccine, since no major difference was found when the immunisation histories of children admitted to hospital with such conditions were compared. No convincing evidence that DTP caused major neurological damage emerged from this large and lengthy study.
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PMID:A 7-year survey of disorders attributed to vaccination in North West Thames region. 613 93

Brown Norway rats have been actively sensitized against hen ovalbumine mixed with anti Bordella pertussis vaccine. After ten to twelve days, IgE are detected in the blood, but no precipitins. Anaphylactic shock induced by i.v. injection of 1 mg.100 g-1 body weight of ovalbumine is caracterized by a vascular collapse, the animal dying in about 15 minutes. This collapse is identical with the same general anaphylactic reaction as observed in the Wistar rats, which have large amounts of precipitins in the blood.
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PMID:[Anaphylactic shock in brown Norway rats with reagins and no precipitins in the blood (author's transl)]. 700 96

An assay employing patterned laminin substrata was used to screen for compounds that disrupt neurite guidance. One molecule, pertussis toxin, caused neurites to wander from patterns that normally guided them, yet had no significant effect on rates of neurite outgrowth. Wandering was greatest on patterns requiring frequent guidance (e.g., laminin stripes with periodic gaps). Surprisingly, the B oligomer of pertussis toxin, which lacks the subunit that inactivates G proteins, was equipotent at disrupting neurite guidance. Pertussis toxin probably acts by binding cell surface carbohydrates, since neurites lacking complex-type N-linked oligosaccharides were insensitive to the effects of the toxin. The B oligomer also blocked growth cone collapse induced by a brain membrane-derived factor; such factors are thought to act as repulsive guidance cues in vivo. That a single reagent can inhibit neuronal responses to both attractive and repulsive guidance cues suggests that such cues may share signaling pathways.
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PMID:Pertussis toxin specifically inhibits growth cone guidance by a mechanism independent of direct G protein inactivation. 761 32

The neuronal growth-associated protein GAP-43 is expressed maximally during development and regeneration, and is enriched at the cytosolic surface of the growth cone membrane. GAP-43 can activate the GTP-binding protein G(o) which is also a major component of the growth cone membrane. These findings have led to the hypothesis that GAP-43 might modulate neurite outgrowth by altering G-protein activity. Here we define the sequence requirements for GAP-43 amino terminal peptide stimulation of G(o), and test these peptides as potential modulators of neurite outgrowth. The first 10 amino acids of GAP-43, Met-Leu-Cys-Cys-Met-Arg-Arg-Thr-Lys-Gln, stimulate G(o). Substitutions at particular residues reveal that cys3, cys4, arg6, and lys9 are critical, but arg7 is not. Both the GAP-43(1-10) peptide and the G-protein-activating peptide mastoparan induce growth cone collapse and inhibit neurite extension from embryonic chick dorsal root ganglion and retinal neurons. This is likely to be mediated by G-proteins: pertussis toxin blocks the inhibition, and mutant peptides that do not activate G(o) do not alter outgrowth. In contrast to the case with embryonic chick dorsal root ganglion cells, neurite outgrowth from N1E-115 neuroblastoma cells is stimulated by GAP-43(1-10). This is probably also a G-protein-mediated event because it is blocked by pertussis toxin, because the sequence requirements match those for G(o) stimulation, and because mastoparan stimulates outgrowth from these cells. The longer GAP-43(1-25) peptide does not alter neurite outgrowth unless the cells are permeabilized, suggesting an intracellular site of action. These data identify a novel set of compounds that modulate neurite outgrowth, and also support the notion that GAP-43 can alter neurite extension by modulating pertussis toxin-sensitive G-protein activity in the growth cone.
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PMID:GAP-43 amino terminal peptides modulate growth cone morphology and neurite outgrowth. 808 50


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