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)

Some yeast mannans increased vascular permeability and caused anaphylaxis-like reactions, fatal in some cases, in nonsensitized CFW mice. In SWR mice deficient in the complement system component C5, anaphylactic shock did not develop after the injection of mannans but was readily induced by goat serum after the mice had been sensitized with Bordetella pertussis and goat serum. The observed biological activity of the yeast mannans appears to depend upon the alpha(1 --> 2) and alpha(1 --> 6) linkages in their main chain. Their relative inactivity in C5-deficient mice and the consumption of whole hemolytic complement after their addition to normal mouse serum suggest that yeast mannans may activate late-acting complement components to produce anaphylatoxin from complement components C5 and C3.
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PMID:Fatal anaphylaxis-like reaction induced by yeast mannans in nonsensitized mice. 411 79

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

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

The difficulties involved in quantitating passive cutaneous anaphylaxis led us to examine the rat paw as a site for passive anaphylaxis and to define optimum conditions for passive paw anaphylaxis. Generation of homocytotropic antibodies in a number of different rat strains revealed that female Brown Norway rats were excellent producers of high titre antisera after only a single injection of antigen and Bordetella pertussis. Injection of ratpaws with diluted antisera followed by short (1-2 h) or long (72 h or more) sensitization periods showed that maximum paw swelling occurred 15 min after antigen challenge. Retention of tissue sensitizing capacity in the paw for greater than 35 days but loss of this capacity following heating of antiserum at 56 degrees C, indicated that the rat homocytotropic antibodies involved in passive paw anaphylaxis belong to the IgE class. Experiments using mepyramine, methysergide and diethylcarbamazine showed that 5-hydroxytryptamine is the most important mediator of passive paw anaphylaxis after both a short (2 h) and a long (72 h) sensitization procedure. Passive paw anaphylaxis in the rat is at least as easy to perform as passive cutaneous anaphylaxis, results can be obtained more rapidly and accurate measurement of paw thickness is not difficult. The procedure is a viable alternative to passive cutaneous anaphylaxis and may offer advantages over the latter method especially in the search for, and rapid assessment of, anti-allergic compounds.
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PMID:Passive paw anaphylaxis in the rat. Optimum conditions for use in studies on immediate hypersensitivity. 625 14

Homocytotropic antibody (HTA) production in pigs was stimulated by sensitization with alum precipitated equine serum or with equine serum in Freund's complete adjuvant. Two doses of appropriate antigen were given in 7 days interval simultaneously with heat inactivated suspension of Bordetella pertussis organisms. HTA were detected in 6 of 10 pigs sensitized with alum precipitated serum and in 4 of 6 pigs sensitized with serum in Freund's complete adjuvant. In pigs sensitized with alum precipitated serum HTA appeared at day 6 after the first antigen administration. In pigs sensitized with serum in Freund's complete adjuvant HTA appeared at day 18 after the first antigen administration. Time course of appearance of HTA was about 10 days in both groups. Alum precipitated serum elicited considerably higher titres of HTA than equine serum in Freund's complete adjuvant. The passive cutaneous anaphylaxis activity of the HTA sera was located in the 7S fraction.
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PMID:[Dynamics of homocytotropic antibody production in pigs]. 625 32

A mouse model is presented giving boosterable IgE antibody responses preceding the IgG antibody responses without using adjuvants. Groups of CBA mice were injected subcutaneously with minute doses of penicilloyl bovine gammaglobulin, 3.8-94 ng daily for one or two 10-day periods. Some groups of animals were simultaneously given Bordetella pertussis bacteria intraperitoneally. The IgE antibody responses were recorded with passive cutaneous anaphylaxis (PCA) in rats as well with RAST. IgG antibody responses were determined with a double antibody assay. An overall good agreement between the antibody activity in the PCA and RAST was seen, both tests showing boosterable IgE antibody responses. Some discrepancies between the two tests are discussed.
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PMID:Boosterable IgE antibody response in mice without the use of adjuvant. 627 7

The effect of dermonecrotic toxin (DNT), fimbrial hemagglutinin (FHA), K-agglutinogen, lipopolysaccharide (LPS), and pertussigen from Bordetella pertussis on the production of IgE and IgG1 antibodies to hen egg albumin (Ea) was investigated in C57BL/6 mice. The IgE antibody contents were determined by passive cutaneous anaphylaxis (PCA) in the skin of Lewis rats, while the IgG1 antibody contents were determined by PCA reactions on the skin of mice using sera that had been heated for 3 hr at 56 C to destroy the IgE antibodies. Among the B. pertussis components tested, pertussigen was the most effective adjuvant for increasing the IgE and IgG1 antibodies to Ea. LPS also moderately increased both types of antibodies, and FHA slightly increased the IgG1 titers. When LPS was given 5 days before Ea, it suppressed both IgE and IgG1 titers while FHA had only slight adjuvant action on both type of antibodies. When each of the components was tested for its ability to modify the adjuvant action of pertussigen, it was found that only DNT interfered significantly with the adjuvanticity of pertussigen when given on the day of immunization with Ea. When the components were given 5 days before Ea, DNT produced significant suppression of only the IgG1 response. LPS, FHA, and K-agglutinogen did not significantly affect the adjuvant action of pertussigen.
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PMID:Effects of Bordetella pertussis components on IgE and IgG1 responses. 632 10

Rats were sensitized with a single intraperitoneal dose of bovine serum albumin in alhydrogel plus Bordetella pertussis vaccine, and local anaphylaxis was elicited in the paw by soluble antigen 2 weeks later. The response was mainly due to IgE-type antibodies and proved to be highly sensitive to beta-adrenoceptor agonists. Dexamethasone inhibited the response after a lag phase. Methysergide, disodium chromoglycate, diethylcarbamazine, BW 775/c, nordihydroguarjaretic acid, and FPL 55712 were also suppressive, while mepyramine was without effect. A synergism between methysergide and FPL 55712 was shown. Active local paw anaphylaxis appears to be adequate and easily applicable for large-scale screening of anti-allergic drugs.
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PMID:A new method of testing anti-allergic drugs. 634 Dec 56

Passive cutaneous anaphylaxis (PCA) sensitivity and IgE antibody production were examined in rats from four different outbred colonies: Wistar A, Wistar B, Sprague-Dawley, and Donryu. PCA sensitivity was the highest in Wistar B and the lowest in Wistar A rats using anti-Ascaris, antibovine serum albumin, and anti-Clonorchis sinensis IgE antibodies. The PCA sensitivity related inversely to the reverse PCA reaction with rabbit antirat IgE antibody, suggesting that preexisting IgE molecules on the mast cells in the skin interfered with the PCA reaction. However, the skin sensitivity to compound 48/80 was comparable in rats from the four colonies indicating the same sensitivity to nonimmunological stimulation. Ability of rats to produce IgE antibody was tested by immunizing them with dinitrophenol-coupled Ascaris extract and Bordetella pertussis adjuvant. Essentially no difference in antidinitrophenol-coupled Ascaris extract IgE antibody production was observed among animals from the different colonies.
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PMID:Sensitivity of passive cutaneous anaphylaxis in rats. I. Inverse relationship between PCA sensitivity and amount of IgE present on mast cells. 634 5

Lotifazole (F 1686) - 4-phenyl-2-(2',2',2-trichloroethoxycarboxamido) thiazole - has a range of anti-inflammatory activities in animals that differs from the activities of classic non-steroidal drugs. It reduces carrageenin-induced oedema in rats, UV-induced erythema in guinea pigs, and Arthus pleurisies in rats only at high doses. It does not affect Freund's-adjuvant polyarthritis, and it only slightly affects passive skin anaphylaxis in rats and anaphylactic shock in guinea pigs. Lotifazole does not greatly inhibit prostaglandin synthesis. However, at low doses and after various conditions of treatment, F 1686 reduces PPD- and Bordetella- pertussis-induced delayed-hypersensitivity pleurisy in guinea pigs and rats, respectively, and contact hypersensitivity reactions to picryl chloride and oxazolone in mice. Its action on the two models of delayed-hypersensitivity pleurisy is reflected in a decrease of the pleural exudate and of the number of mononuclear cells in the focus of inflammation. At active doses, Lotifazole does not cause changes in the differential leukocyte count in normal animals. It appears, furthermore, to be a T-lymphocyte stimulant.
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PMID:Lotifazole (F 1686), a non-steroidal anti-inflammatory agent with an unusual pharmacological spectrum. 670 14


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