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)

Attempts were made to manipulate specific responses of baboons to protect them from infection with Schistosoma mansoni. In Experiment 1, eosinophilia was induced in naive baboons with Trichinella spiralis larvae given intravenously before intraperitoneal injection of globulin fractions from S. mansoni-infected baboon sera and subsequent percutaneous exposure to S. mansoni cercariae. In Experiment 2, baboons with 8- or 32-week-old primary S. mansoni infections received T. spiralis i.v. before an S. mansoni challenge. In experiments 3 to 5 respectively, naive baboons received intramuscularly before challenge: formalin-fixed S. mansoni schistosomula, with Bordetella pertussis as an adjuvant; a preparation of S. mansoni adult worm teguments; and a preparation of IgE-immune complexes obtained from S. mansoni-infected rat sera, with Freunds Complete Adjuvant. Minor, but statistically insignificant, protection was obtained in Experiments 2 (32-week infections) and 3, but was far less than that given by intact, irradiated living vaccines. There are signs on the horizon of non-living vaccines protecting rodents against S. mansoni infection and it would be prudent, as with drugs, to test these in primates before proceeding to man. The results of our experiments, though essentially negative, should help the design of any future vaccine trials in primates.
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PMID:Attempts to manipulate specific responses to induce resistance to Schistosoma mansoni in Kenyan baboons (Papio anubis). 403 58

Immunogenicity of culture filtrates of various air-born fungi with respect to reaginic antibody formation was tested in the rat. Animals immunized with two successive injections of culture filtrates of fungi with the aid of Bordetella pertussis vaccine as an adjuvant produced fairly high titers of reaginic antibodies of the IgE class. Little cross-reactivity was detected between reagins induced by different strains of fungi. The reaginic immunogenicity was only found in the culture fieltrate produced by the surface culture, in which large amounts of conidia were formed, but not in the filtrate obtained from the shaking culture, in which only mycelial components were growing. Therefore, it was suggested that allergens responsible for the reaginic antibody formation derive from the conidium but not from the mycelium. The results indicate that air-born fungi are potentially immunogenic for production of reaginic antibodies, and further suggest their causative roles in human atopic diseases.
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PMID:Immunogenicity of fungi for the production of reaginic antibody in the rat. 437 63

Passive cutaneous anaphylaxis (PCA) produced by antigen challenge to antibody-sensitized rats were interfered with by prior treatment with pertussis toxin, an islet-activating protein (IAP). The degree of interference was dependent on the dose and injection time of IAP; the effect of IAP developed slowly, with a maximal effect being observed 3 days later. Inhibition of PCA by IAP was associated with a decrease in histamine release from peritoneal mast cells, making it very likely that the process affected was mast cell secretion. Much less histamine was discharged in vitro, in response to certain membrane receptor (e.g. IgE receptor) stimulation, from mast cells that had been exposed to IAP than from the cells not exposed. Such an inhibitory effect of IAP was not observed when histamine release was provoked by a calcium ionophore without mediation of membrane receptors. IAP was a stronger inhibitor of histamine release than beta-adrenergic agonists. Further inhibition was produced when a beta-agonist was added to IAP-treated mast cells. The increase in the cellular content of cyclic AMP was associated with beta-agonist-induced, but not with IAP-induced, inhibition of histamine release. Thus, IAP inhibited histamine release by a mechanism in which metabolism of cyclic AMP was not directly involved.
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PMID:Suppression of passive cutaneous anaphylaxis by pertussis toxin, an islet-activating protein, as a result of inhibition of histamine release from mast cells. 614 11

IgE antibodies to a cephalothin preparation were produced in mice which had been immunized with cephalothin-Ascaris extract conjugate mixed with Al(OH)3 gel plus Bordetella pertussis. Mice which had been irradiated just before receiving the booster injection wtih the conjugate showed higher IgE antibody levels against the preparation in comparison with unirradiated mice. The specificities of IgE antibodies against the preparation were examined with an inhibition test of passive cutaneous anaphylactic (PCA) reaction. The intensity of the PCA reaction evoked by the cephalothin preparation in the rats was substantially or partially reduced by a pretreatment of the animals with an injection of a cephalothin preparation from another source or a cephaloridine preparation. Meanwhile, a prior injection of a cefazolin, a 7-aminocephalosporanic acid, a benzylpenicillin (PcG) preparation, or an aminobenzylpenicillin preparation into the animals showed only weak or no influence on the PCA reaction. These results suggest that the acyl side chain of cephalothin plays an important role as eliciting antigenic determinant in the PCA reaction. The difference in the antigenic specificity between the cephalothin and PcG preparation is also discussed.
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PMID:IgE antibodies produced in mice instrumental in analyses of antigenicity of cephalothin preparation. 615 86

Histamine release from isolated rat mast cells from non-immunized and immunized Hooded Lister rats was induced by compound 48/80. The histamine release was decreased with a lower maximum at the optimal concentration of 48/80 when using cells from immunized rats compared to non-immunized control rats. The stimulation of IgE antibody production, after immunization using B. pertussis as an adjuvant was also accompanied by an elevation of total serum IgW. The 48/80 induced histamine release from Sprague Dawley mast cells was not inhibited by immunization. Non-antibody IgE showed a non-competitive inhibition of 48/80 induced histamine release when myeloma IgE was incubated with mast cells from both Hooded Lister and Sprague Dawley rats. The results indicate the existence of different receptors for IgE and 48/80.
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PMID:Effect of sensitization and non-antibody IgE on 48/80 induced histamine release from isolated rat mast cells. 615 31

Sprague Dawley (SD) rats were immunized with various penicillin-ovalbumin (OvA) in combination with aluminum hydroxide (alum) and thimerosal-killed Bordetella pertussis for the purpose of obtaining rat anti-penicillin IgE sera. In the rat 60-hour passive cutaneous anaphylaxis (PCA) reaction and the hapten inhibition test, a weak cross reaction between penicillin G (PCG) and ampicillin (ABPC) was observed, but not cross reaction was observed between sulbenicillin (SBPC) and other penicillins. Rat anti-6-formamidopenicillanic acid (FPC) IgE serum reacted with PCG-bovine gamma globulin (BGG), ABPC-BGG and SBPC-BGG, but FPC-BGG did not react with rat anti-PCG, anti-ABPC and anti-SBPR IgE sera and the PCA reaction between anti-FPC IgE sera and FPC-BGG was inhibited by FPC, PCG, ABPC and SBPC. These results indicate that the antigenic active sites of PCG, ABPC and SBPC are limited to the acyl side chain moiety of penicillins, while the antigenic active site of FPC is confined to the penicilloyl moiety of the penicillin.
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PMID:IgE antibodies for penicillins and cephalosporins in rats. II. Antigenic specificity of rat anti-penicillin-OvA IgE sera. 616 3

Sprague Dawley (SD) rats were immunized with various cephalosporin- and penicillin-ovalbumin (OvA) in combination with aluminium hydroxide (alum) and thimerosal-killed Bordetella pertussis. Anti-cephalosporin IgE antibody production was inferior to anti-penicillin IgE antibody production. Cefsulodin (CFS), sulbenicillin (SBPC) and alpha-sulfophenyl acetic acid (SPAA) cross-reacted with each other but did not react with cephaloridine (CER), cefazolin (CEZ) and penicillin G (PCG). CER and PCG slightly cross-reacted with each other but did not cross-react with the others tested. Anti-CFS and anti-SBPC IgE sera were related specifically to the SPAA moiety.
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PMID:IgE antibodies for penicillins and cephalosporins in rats. III. Antigenic specificity of rat anti-cephalosporin-OvA IgE sera. 616 4

Islet-activating protein (IAP) is a new active substance purified from the culture medium of Bordetella pertussis. The active protein possesses a molecular weight of 77,000 and an isoelectric point of pH 7.8. The nature of IAP-action is characterized by enhancement of insulin secretory response to glucose and other stimulants. A single injection of IAP into spontaneous diabetes rats resulted in normalization of their glucose intolerance over a period of a month. Acute and chronic animal toxicity tests showed that LD50 of IAP was 127 micrograms/kg in mice and 144 micrograms/kg in rats. After these animal experiments, phase 1 studies were designed and undertaken to establish dosage, duration of action and other factors. IAP of 0.5 micrograms/kg or 1.0 micrograms/kg did not bring about any serious toxic or adverse effects in five volunteers. On the 4th day of a single injection of IAP, insulin secretory response was proved to be enhanced. Follow-up studies showed that the IAP-action continued over a month or at most two months. Two features of IAP, i.e., the enhancement of insulin secretory response and the long duration of the action, was confirmed in healthy persons as well as in animals. As expected, IAP has a strong antigenic reaction resulting in formation of IgG antibody and possibly IgE antibody. The antigenicity of IAP causes some hindrance to clinical usefulness. For avoidance of anaphylactic reaction, IAP should be given repeatedly with care. The problem concerning antigen-antibody reaction should be overcome as soon as possible before the clinical use of IAP as a medicament.
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PMID:Effects of islet-activating protein (IAP) on blood glucose and plasma insulin in healthy volunteers (phase 1 studies). 624 81

In Hooded Lister rats the primary IgE antibody response induced by immunization with antigen and adjuvant may be enhanced either specifically by a further dose of antigen (booster response) or non-specifically by infection with helminth parasites (potentiated response). The initial immunizing technique can influence the occurrence and level of these enhanced responses and here we describe the effect of using different adjuvants in the priming event. Although the level of the primary response was broadly similar following immunization with egg-albumin and the adjuvants Bordetella pertussis aluminium hydroxide or Freund's complete adjuvant, the booster response was inhibited and the potentiated response intensified in animals immunized with the latter two adjuvants. A significant IgE booster response could only be obtained if B. pertussis had been used in the initial immunization. When aluminium hydroxide was adsorbed to B. pertussis it was found to have the same inhibitory effect on subsequent booster responses as when it was adsorbed to antigen. These results are discussed in relation to the intricacies of IgE production in the present model and to more general mechanisms of adjuvant action.
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PMID:Adjuvants in the induction and enhancement of rat IgE responses. 624 78

The effects of 16(S)-methyl-20-methoxy-PGE2 (YPG-209) on hypersensitivity reactions were investigated in the rat, guinea-pig and mouse. Intravenously administered YPG-209 was 150 times as potent as disodium cromoglycate (DSCG) in the inhibitory effect on the IgE(mouse)-mediated 24 hr rat PCA. When administered intravenously to guinea-pigs, YPG-209 inhibited significantly the IgE (guinea-pig)-mediated 8 day guinea-pig PCA, whereas DSCG exhibited no significant inhibitory effects. The oral doses of YPG-209 diminished both histamine and 5-hydroxytryptamine hypersensitivity of the Bordetella pertussis-treated mice. These results suggest that YPG-209 exhibits not only the prevention of mediator release but also the antimediator effect in laboratory animals.
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PMID:Inhibition of hypersensitivity reactions by 16(S)-methyl-20-methoxy-PGE2 (YPG-209) in animals. 625 64


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