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 effects of prostaglandin E1, E2, F2alpha (PGE2 PGF2alpha), isoproterenol, epinephrine, norepinephrine, salbutamol, practolol, atropine, aminophylline, and corticosterone on the hypersensitivity to anaphylaxis, histamine, and serotonin in Bordetella pertussis-treated mice and propranolol-treated mice were investigated. Female HLA-SW (ICR) mice, 27-29 gm, were injected with pertussis vaccine intravenously 4 days before challenge with antigen, histamine, or serotonin. Alternatively, instead of pertussis vaccine, propranolol was injected intraperitoneally 45 min before histamine challenge. Test drugs were administered intraperitoneally 15 min before challenge. PGE1 and PGE2 at a narrow range of between 10 and 100 mug and epinephrine at 100 mug protected both pertussis- and propranolol-treated mice. Isoproterenol (25 mug) and aminophilline (800 mug) protected beta-blocked mice, but did not protect pertussis-treated mice even with very high doses (1,000 and 3,2000 mug, respectively), although salbutamol (500 mug) did. PGF2alpha, norepinephrine, and atropine were not protective at all. Practolol, a beta 1-blocker, given intraperitoneally 30 min before histamine neither sensitized normal mice nor changed the effect of isoproterenol or salbutamol in pertussis-treated mice. Corticosterone 10 mg/kg reduced the number of deaths from histamine in beta-blocked mice, but not in pertussis-treated mice. The protective effect is discussed in connection with probable effects of the drugs on intracellular cyclic adenosine monophosphate (cAMP) levels.
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PMID:Histamine hypersensitivity in mice induced by Bordetella pertussis or pharmacologic beta adrenergic blockade. Effects of adrenergic, cholinergic, and other drugs. 0 37

The effects of the route of the injection and adjuvants on the immune response of guinea pigs were investigated at various stages of immune response to tetanus toxoid. Delayed-type hypersensitivity (DH) was observed as the first immune response to the toxoid before initiation of antitoxin production. The DH reaction was weak when plain toxoid was administered subcutaneously. Water-in-oil in water (w/o/w) enhanced greatly the reactivity of the immunized animals; pertussis vaccine, endotoxin and aluminium showed adjuvanticities in this order. The foot pad (fp) injection of plain toxoid promoted remarkably the induction of DH. The reactivity was enhanced considerably by w/o/w and to a less extent by aluminium. However, pertussis vaccine showed an adverse effect on DH by the fp route. Active cutaneous anaphylaxis (ACA) induced by the subcutaneous route was enhanced by w/o/w, endotoxin, pertussis vaccine and, to a less extent, by aluminium. The fp route compared with the sc route enhanced ACA by plain toxoid; w/o/w and aluminium but not endotoxin and the vaccine showed adjuvanticities. The influences of adjuvants and the route of injection on Arthus reactions were inconsistent. The effect of adjuvants on antitoxin production was quite different from that on DH when antitoxin was produced abundantly. Aluminium showed consistently a potent adjuvanticity, but activities of w/o/w, endotoxin and pertussis vaccine were inconsistent 4-6 weeks after the primary stimulus by the subcutaneous route. The adjuvant effect became less significant in the secondary response. The fp route was more favorable for antitoxin production than the subcutaneous route with most adjuvants except pertussis vaccine added to tetanus toxoid. Antitoxin production by plain toxoid was very poor when administered intraperitoneally; aluminium and w/o/w but not endotoxin showed a remarkable adjuvanticity for the antitoxin production.
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PMID:Studies on adjuvants for human prophylactics. II. Influence of the route of injection on the activity of adjuvants to tetanus toxoid in guinea pigs. 15 4

The single i.p. injection of 2.5 times 10-8 killed B. pertussis cells protected 23 out of a group of 24 NMRI mice (95.8%) against the subsequent intracerebral infection, whilst 13 out of 24 mice (54.2%) survived the intracerebral challenge with virulent B. pertussis cells after prior oral administration of 2.5 times 10-11 killed B. pertussis cells, as demonstrated by the mouse protection test. Similar treatment with non-specific substances, such as egg white and saline, did not result in any increase of resistance. Systemic anaphylactic hypersensitivity to bovine serum albumin could also be achieved, when either both the protein antigen and the B. pertussis vaccine were given by the oral route or when the B. pertussis vaccine was injected intraperitoneally into mice which had received the soluble protein antigen by the oral route. Such effects were not produced at all in the reverse situation, when the B. pertussis vaccine was orally administered in mice, which were given the soluble protein antigen by the intraperitoneal route. After oral inoculation of 6 times 10-11 killed B. pertussis cells neither splenomegaly nor blood lymphocytosis became detectable. It is still unknown, in which manner the orally administered B. pertussis vaccine effects protection against the intracerebral infection with virulent bacteria as well as susceptibility for systemic anaphylaxis. The data presented do not favor the view that those effects are due to the phenomenon of persorption.
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PMID:Studies on the immunizing capacity of orally administered particulate antigens. I. The efficiency of killed Bordetella pertussis cells. 16 35

The effects of exogenous nucleotides on the histamine hypersensitivity of pharmacologically beta-blocked mice were investigated. Female HLA-SW (ICR) mice, 27-29 gm, were injected intraperitoneally with 20 to 100 mug of propranolol 45 min before intraperitoneal challenge with 1 mg histamine. These animals had a mortality which averaged approximately 80%. At various time intervals before histamine, doses of from 0.5 to 12 mumoles of nucleotides were administered intravenously. Noncyclic nucleotides, adenosine, adenosine 5'-monophosphate (AMP), and guanosine 5'-monophosphate (GMP) showed clear, dose-response protection against histamine death of propranolol-treated mice when they were given 45 to 90 min before histamine. Cyclic AMP showed significant protection only when it was given at a dose of 8 mumoles 45 to 90 min before histamine, and lower or higher doses gave equivocal or no protection. Cyclic GMP WAS Not protective at any dose tested. Propranolol treatment also produced enhanced sensitivity to passive systemic anaphylaxis. Mice were passively sensitized by intraperitoneal injection of mouse anti-egg albumin antibody 6 hr before intravenous challenge with 0.5 mg egg albumin. The mortality from anaphylaxis in the group treated with 20 mug propranolol 45 min before antigen challenge increased to 83%, while that of the group not given propranolol was only 10%. Nucleotides were given intravenously 45 min before antigen challenge. The nucleotides that protected mice from death due to histamine challenge also protected them from death due to systemic anaphylaxis. These protective nucleotides were the same nucleotides that had been reported previously to be protective against Bordetella pertussis-induced hypersensitivity to histamine and anaphylaxis.
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PMID:Hypersensitivity to histamine and systemic anaphylaxis in mice with pharmacologic beta adrenergic blockade: protection by nucleotides. 18 34

Regarding the adjuvant activity of gram-negative bacteria we have to distinguish at least 4 different potencies, i.e., 1) increase in the production of circulating antibodies during the primary and secondary immune responses; 2) induction of susceptibility to systemic anaphylaxis; 3) prompt production of experimental "allergic" diseases, and 4) increase in resistance to infections. Although all gram-negative bacteria contain several structural components with adjuvant potencies, the immunopotentiating effectiveness of the corresponding whole bacteria becomes--with the exception of killed cells of Bordetella pertussis--only detectable to a weak degree.
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PMID:[Adjuvant activity of gram-negative bacteria and their structural components (author's transl)]. 19 40

The authors describe the inhibiting action of mannitol after repeated administration of low subcutaneous doses in a number of experimental immunological models. For example, in the rat it produces a reduction of the secondary arthritis of Freund's adjuvant polyarthritis and also of the pleurisy due to Bordetella pertussis hypersensitivity. In the mouse it reduces the reaction of delayed hypersensitivity to sheep red cells. Its action is also marked against ovalbumin-induced active skin anaphylaxis in the albino guinea-pig and on IgE synthesis in the rat. Moreover, after several injections it produces a reduction of carbon phagocytosis in the mouse. At the doses at which the effect appeared, no action could be found on various models of acute non-immune inflammation, diuresis, blood pressure, hematocrit and protein and plasma sodium levels.
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PMID:Action of mannitol in various immunological experimental models. 22 21

The intensity of anaphylactic shock was lower in C3H mice carrying a methylcholanthrene-induced tumour (McC3) than in their normal counterparts when immunized with ovalbumin and challenged i.v. after 14 days. This tumour-associated inhibitory effect on active systemic anaphylaxis was exerted mainly on events occurring after homocytotropic antibody synthesis because the serum titres of these antibodies were comparable in normal and tumour-bearing animals. In addition, passive systemic anaphylactic reactions were suppressed in animals carrying the tumour and the sensitivity of these animals to challenge with histamine and serotonin mixtures was also reduced. The presence of a growing McC3 tumour did not, however, diminish the amine-sensitizing effect of treatment with Bordetella pertussis vaccine. The McC3 tumour inhibited the generation of passive cutaneous anaphylactic reactions, an effect that was also exerted by a tumour extract, particularly when administered to the recipients shortly before antigen challenge. Thus immediate hypersensitivity reactions, like a variety of other immunological processes, can be inhibited by tumour products which by compromising the immune status of the host might permit tumour growth. The nature of the inhibiting factor is unknown, except that it is probably not the amine-degrading enzyme histaminase. In addition, which it is uncertain whether the inhibitory effect is exerted directly or indirectly, the possible importance of prostaglandins in the phenomenon is discussed.
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PMID:Tumour-associated inhibition of immediate hypersensitivity reactions in mice. 40 15

Reaginic antibody in ascitic fluid was isolated from mice immunized with ovalbumin and TAl(OH)3 or with avalbumin and pertussis adjuvant. Partial purification of this reagin by ammonium sulphate precipitation, gel filtration, and ion-exchange column chromatography yielded a gammaglobulin fraction highly active in the passive cutaneous anaphylaxis reaction. This was identical in purity and specific activity to a fraction of partially purified reagin isolated from mouse antiserum. The recovery of reaginic activity after purification from ascitic fluid was 19 per cent compared to the 7-8 per cent recovery from anti-serum. These studies demonstrate that ascitic fluid in mice immunized with methods known to produce reaginic antibody provides an excellent source of mouse IgE.
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PMID:Induction and yield of reaginic antibodies in mouse serum and ascitic fluid. 81 76

IgE synthesis has been reported to be inhibited by theophylline and dibutyryl cyclic adenosine monophosphate and increased by pertussis vaccine. This study was done to determine if chronic beta-adrenergic blockade affects IgE antibody production. 72 C57BL/10J mice were sensitized with egg albumin (EA, 125 microng). Groups included: (1) EA alone; (2) EA + complete Freund's adjuvant (FA); (3) EA + B. pertussis (8 X 10(9) organisms); (4) EA + propranolol (0.5 mg/kg) 3 times/day; (5) EA + FA + propranolol; (6) saline alone. Booster was given on day 49. Group 1, given EA alone, failed to develop any passive cutaneous anaphylaxis (PCA) antibodies even after booster, whereas the 72-hour PCA titers ranged from 1/64 to 1/256 for groups treated with propranolol and propranolol + FA, respectively. The results suggest that chronic beta-adrenergic blockade enhances IgE antibody formation.
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PMID:Effect of beta-adrenergic blockade, pertussis vaccine and Freund's adjuvant on reaginic antibody response in mice. 87 Apr 38

In the early stages of anaphylactic shock of rats pretreated with Bordetella pertussis vaccine, a prompt and parallel activation of the factor XIIa-dependent intrinsic coagulation, kinin generation, and fibrinolytic acticity was observed. The coagulation studies, the similarity of anaphylactic results with those produced by a single injection of ellagic acid, and the effective inhibition of the anaphylactic and the ellagic acid-induced activation of these pathways by lysozyme all suggest that factor XII itself becomes activated in rat anaphylaxis. As the reaction proceeded, considerable anticoagulant activities emerged, but the bradykinin and the plasminogen activator levels even further increased. During the first 10 min of anaphylactic shock, factor XII was partly consumed and this was prevented by epsilon-aminocaproic acid infusion. The results show that in pathological conditions such as anaphylaxis there is an intimate in vivo interaction among the three factor XIIa-dependent pathways.
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PMID:Activation and consumption of Hageman factor in the anaphylactic shock of the rat. 96 6


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