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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sprague Dawley rats were sensitized with 20 microgram or 100 mg egg albumin (using pertussis vaccine as adjuvant). Mast cells isolated from the former group of animals showed a higher degree of histamine release upon challenge in vitro with egg albumin than those from the latter group. Using the lower amount of antigen for immunization mast cells from Hooded Lister rats showed an even higher degree of histamine release induced by antigen. An increased antigen-induced histamine release was associated with an increased spontaneous and phosphatidylserine-induced histamine release. Histamine release induced by phosphatidylserine was found to be specific in so far as it was calcium dependent and theophylline-inhibited. The basal level of cyclic AMP in mast cells was significantly depressed by sensitization. There was a relationship between the cyclic AMP/cyclic GMP ratio and the degree of spontaneous, phosphatidylserine-induced and anaphylactic histamine release. The results suggest that sensitization induces an increased release of histamine not only to the specific antigenic stimulus but also to more unspecific stimuli. Concomitantly there is a fall in the cyclic AMP/cyclic GMP ratio. The relationship between these two phenomena is discussed.
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PMID:Effect of sensitization on spontaneous and phosphatidylserine-induced histamine release and on cyclic AMP and GMP levels in isolated rat mast cells. 9 6

Inbred Hooded Lister rats were immunized with egg albumin with B. pertussis vaccine used as an adjuvant. The serum levels of total IgE and IgE antibody (egg albumin specific) were determined by radioimmunoassay techniques before and after immunization. The basic level of total IgE in serum was 560 +/- 110 ng/ml. After immunization a maximal peak at day 11 of 1940 +/- 160 ng/ml was registered. Anti-egg albumin IgE antibody showed a maximum around day 13 of 75 +/- 11 units/ml. Pleural mast cells were isolated on Ficoll between day 14 and 20 after immunization. A significant negative correlation between the basic total IgE level and histamine release by antigen (egg albumin) was found and also a significant positive correlation of specific IgE antibody (determined at day 11) and histamine release. The correlation between IgE level and histamine release was slightly improved if instead the ratio of specific IgE antibody over total IgE was used.
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PMID:Relationship between serum IgE levels and anaphylactic histamine release from isolated rat mast cells. 9

The time courses of production of IgE and IgGa homocytotropic antibodies were measured in Wistar rats during a primary and secondary response to egg albumin with pertussis or Freund's adjuvants. An anamnestic IgE antibody response occurred in animals previously sensitized to antigen with killed Bordetella pertussis as adjuvant. IgGa antibodies were formed in the primary response with Freund's complete adjuvant only, but were found during the secondary response with all adjuvants used. The time courses of formation of IgE and IgGa antibodies were very different during the secondary response. The production of both classes of antibody to egg albumin was studed in Wistar and Hooded Lister rats infected with Nippostrongylus brasiliensis. IgGa antibody formation was not potentiated by the infection. However, increased levels of IgE antibody, formed during a secondary response to antigen in infected animals, were consistently higher in both strains than during a primary response.
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PMID:The production of IgE and IgGa antibodies in normal rats and rats infected with Nippostrongylus brasiliensis. 17 91

Primary and booster IgE antibody responses have been elicited in Hooded Lister rats by the intradermal injection or oral administration of very small quantities of egg albumin. Oral immunization was effected by giving antigen by stomach tube or in the drinking water. The minimum primary dose of antigen found to be effective was 1 mug intradermally and 10 mug orally, administered together with an intraperitoneal injection of B. pertussis adjuvant. In rats immunized with these doses secondary responses could be evoked by giving even smaller quantities of antigen, thus 1 ng intradermally or 1 mug orally without adjuvant. Smaller challenge doses were not tried. Large primary doses of antigen (greater than 100 mug) presented by these routes were, on the other hand, found to be inhibitory to the production of secondary IgE responses, this effect being similar to that observed in previously reported intraperitoneal immunization experiments. By contrast with previous experiments, however, tertiary responses could be obtained following immunization by these routes, and we believe this to be reflection of the absorption of smaller and therefore less inhibitory quantities of antigen. Our results are discussed in relation to the control of IgE antibody production, current concepts of the control of antigen absorption through mucosal barriers, and possible implications of the genesis of naturally occurring IgE responses in man.
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PMID:Rat IgE production. II. Primary and booster reaginic antibody responses following intradermal or oral immunization. 17 38

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

The potentiation effect of various adjuvants on the production of guinea-pig IgE was investigated using Freund's complete and incomplete adjuvant, the lipopolysaccharide of Escherichia coli and Salmonella typhosa, Bordetella pertussis, and the nematodes Nippostrongylus brasiliensis and Ascaris suum. While all the antigens had a variable effect on the potential of the IgG response, only infection with A. suum resulted in an enhanced IgE response to the antigen, egg albumin. Maximum potentiation occurred when primary immunization and nematode infection were accomplished simultaneously.
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PMID:Effect of Ascaris suum and other adjuvants on the potentiation of the IgE response in guinea-pigs. 50 Jan 18

An animal model of food allergy has been developed in which some aspects of the allergic response could be quantified and the effects of various drugs evaluated. The change in permeability of the intestinal tract of actively sensitized rats, after oral challenge with the sensitizing antigen, was the parameter measured. Rats were sensitized by injection of egg albumin and B. pertussis vaccine to induce reaginic antibody to egg albumin. Two weeks after sensitization, 125I-labelled bovine serum albumin (125I-labelled BSA) was injected intravenously, followed by oral challenge with egg albumin. Pieces of intestinal tissue were obtained and the amount of 125I-labelled BSA determined in a gamma counter. The amount of 125I-labelled BSA in the intestinal tissue of sensitized and challenged rats regularly showed an increase of greater than 100% above values for control rats.
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PMID:Intestinal anaphylaxis in the rat as a model of food allergy. 81 92

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

We were unable, passively, to transfer reactivity against dextran to the skin or peritoneal mast cells of non-dextran-reactive rats, by using serum or material eluted at pH 3 from mast cells of spontaneously dextran-reactive rats. When the dextran-reactive donor rats had also been immunized against egg albumin (EA) with pertussis vaccine (inducing IgE anti-EA antibody), passive sensitivity against EA (but not against dextran) could easily be transferred. The results indicated that the anti-dextran reactivity is not due to IgE antibody. Systemic reactions against dextran and EA differed in pattern, supporting the concept that the two substances acted through different mechanisms.
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PMID:Studies on passive transfer of anti-dextran and anti-egg albumin reactivity in the rat. 101 90

Leukotriene B4 (LTB4) release initiated by interaction of immune complexes (ICs) with Fc gamma RII and Fc gamma RIII receptors on human neutrophils was studied using well-defined complexes. Immune complexes consisting of polyclonal rabbit antibody to human albumin were prepared at equivalence (insoluble complex) and at five times antigen excess (soluble complex). Incubation of human neutrophils with soluble and insoluble ICs led to the synthesis of LTB4 from endogenous arachidonic acid (AA). LTB4 release induced by ICs was markedly inhibited by monoclonal antibodies against either Fc gamma RII or Fc gamma RIII receptor. Treatment of neutrophils with pertussis toxin significantly inhibited the release of LTB4 induced by soluble ICs. However pertussis toxin treatment minimally inhibited the LTB4 release induced by insoluble ICs. Crosslinking of either Fc gamma RII and Fc gamma RIII receptors on neutrophil surfaces induced LTB4 release. This is the first experimental observation showing that both Fc gamma RII and Fc gamma RIII directly induce neutrophil LTB4 metabolism in the absence of exogenous AA. These studies also suggest the involvement of novel pertussis toxin insensitive signal transduction pathways in insoluble ICs stimulation of neutrophils.
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PMID:Insoluble immune complex-stimulated neutrophil leukotriene B4 production is dependent on Fc gamma RII and Fc gamma RIII and independent of pertussis toxin-sensitive signal transduction pathways. 131 7


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