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)

Specific and total IgG and IgE serum levels were measured in Sprague-Dawley rats after immunization with ovalbumin (OA). OA was administered in an aqueous solution, suspended in alum or in Complete Freund's Adjuvant (CFA) with or without simultaneous administration of Bordetella pertussis (Bp). Control groups received only saline, alum or CFA. Specific IgG, total IgG and total IgE were determined by ELISA methods. Specific IgE was biologically evaluated. The highest specific IgG and IgE antibody responses were obtained with OA suspended in alum, while Bp failed to potentiate this response. The low specific response seen with OA suspended in CFA was potentiated when Bp was simultaneously dosed. Total IgE levels were increased in those groups receiving Bp. The contribution of specific IgG or IgE response to the total IgG or IgE levels was not distinguished with this experimental procedure. It can be concluded that immunization with OA suspended in alum induces appreciable increases in specific IgG and IgE antibodies without significantly affecting total IgG and IgE levels.
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PMID:Effect of adjuvants on IgG and IgE response to ovalbumin in rats. 255 66

Stimulation of normal rat splenic T cells with pertussigen (lymphocytosis-promoting factor from Bordetella pertussis) resulted in the release of a soluble factor that enhanced the assembly of N-linked oligosaccharides to IgE-binding factors during their biosynthesis. The glycosylation-enhancing factor (GEF) is a kallikrein-like enzyme and is purified by absorption to p-aminobenzamidine-Agarose followed by elution with benzamidine. Incubation of normal mouse mast cells with affinity-purified GEF or bradykinin, a product of cleavage of kininogen by kallikrein, resulted in the release of histamine and arachidonate from the cells. Passive sensitization of mast cells with mouse IgE antibody, followed by pretreatment of the cells with a suboptimal concentration of GEF, resulted in an enhancement of antigen-induced histamine release. It was found that GEF and bradykinin induced the same biochemical events in mast cells as those induced by bridging of IgE receptors. Both GEF and bradykinin induced phospholipid methylation and an increase in intracellular cyclic AMP (cAMP). Incorporation of 3H-methyl groups into phospholipids and intracellular cAMP levels both reached a maximum 30 sec after challenge with GEF or bradykinin, and then declined to base-line levels within 2 to 3 min. These biochemical events were followed by 45Ca influx and histamine release; 45Ca uptake reached a plateau value at 2 min, and histamine release reached a maximum at 5 to 8 min. The initial rise in cAMP induced by GEF (or bradykinin) was not inhibited by indomethacin, indicating that the activation of adenylate cyclase is not the result of prostaglandin synthesis. In both IgE-mediated and GEF-induced histamine release, inhibitors of methyltransferases, such as 3-deaza adenosine and L-homocysteine thiolactone, inhibited not only phospholipid methylation but also the cAMP rise and subsequent Ca2+ uptake and histamine release. The results indicate that GEF induces activation of methyltransferases and that phospholipid methylation is involved in the cAMP rise, Ca2+ uptake, and histamine release. The induction of the same biochemical events in the same sequence by bridging of IgE receptors and by GEF (bradykinin) supports the hypothesis that receptor bridging induces the activation of serine protease(s) and cleavage products of this enzyme in turn activate methyltransferases in mast cells.
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PMID:Release of histamine and arachidonate from mouse mast cells induced by glycosylation-enhancing factor and bradykinin. 257 23

IgE responses are closely regulated in non-atopic humans and low IgE responder animals. After an initial period of IgE production following antigen exposure, IgE synthesis appears to be actively suppressed. Inhalation of the dust of castor beans induces persistent IgE responses in atopic and non-atopic humans alike. This phenomenon was investigated in animals. Hooded Lister rats were immunized intraperitoneally with different preparations of castor bean. These had been heated for different lengths of time, 60 and 15 mins, to inactivate the toxin ricin. Immunization with as much as 100 micrograms of the extract heated for 60 min failed to produce an IgE response, while injection of 100 micrograms of the extract heated for 15 min produced a marked IgE response to castor bean proteins. Thus the component of castor bean extract which induces the IgE response appears to be heat labile. The IgE potentiating component in castor bean was found to enhance IgE responses to other antigens such as ovalbumin and when 0.8 microgram of an unheated castor bean extract was administered together with an optimal dose of ovalbumin, there was a substantial increase in ovalbumin-specific IgE but not IgG in all animals. In addition, total serum IgE but not IgG increased up to 20-fold. The effect of castor bean was more sustainable than that of an established IgE-specific adjuvant, Bordetella pertussis, and was able to boost an IgE response that had diminished and maintain an ongoing IgE response when re-administered at weekly intervals. In addition, it was possible to reproduce the IgE potentiating effects with purified castor bean ricin at 25 ng/rat. The way that it produces this effect is not known but it is possible that ricin blocks the normal IgE suppressive mechanisms that regulate IgE responses.
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PMID:The effect of the castor bean toxin, ricin, on rat IgE and IgG responses. 259 6

The effect of disodium 4-chloro-2,2-iminodibenzoate (CCA) on IgE antibody response was examined in C3H/A and (BALB/c x C57BL/6J) F1 hybrid mice immunized with low doses of ovalbumin (OA) adsorbed on aluminium hydroxide gel. CCA administered orally at the doses of 5 and 50 mg/kg/day reduced IgE antibody production in these mice as determined by PCA test. High doses of CCA (100 mg/kg/day) given from day 7 before immunization of C57BL mice and during 1 week after immunization of mice with OA and Bordetella Pertussis Vaccine reduced the mortality of these mice subjected to anaphylactic shock on day 7 of immunization. CCA treatment was ineffective in anaphylactic shock of C57BL mice immunized with very high dose of OA, known to elicit little or no IgE antibody production but high IgG antibody response. The treatment of OA-immunized Guinea pigs with one oral dose of CCA (100 mg/kg) did not reduce mortality in protracted anaphylactic shock. Our results demonstrate that CCA inhibits IgE production as well as IgE mediated hypersensitivity reactions in mice.
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PMID:The effect of disodium 4-chloro-2-iminodibenzoate (CCA) on IgE levels and anaphylactic shock. 259 70

Immunoglobulin E antibodies to pertussis toxin (PT-IgE) were demonstrated in 15 of 23 (65%) patients with culture-confirmed pertussis. In 6 individuals there was a low-grade PT-IgE response after 6-9 weeks of disease and in 9 a rapid PT-IgE response, appearing 1-3 weeks after onset of symptoms. The PT-IgE antibody levels in immunized individuals were higher than in the non immunized. Following primary immunization of 23 children with a monovalent whole-cell pertussis vaccine (Burroughs-Wellcome, UK) or with an acellular pertussis vaccine (JNIH-6, Biken, Japan) a late low-grade PT-IgE response was found in 8 (35%). In 7/10 children previously immunized with the JNIH-6, a booster injection 16 months later with the same vaccine resulted in a rapidly appearing PT-IgE antibody response. In contrast, none of 13 children initially immunized with the monovalent whole-cell vaccine and then boostered with either this vaccine or JNIH-6 had detectable PT-IgE antibodies after the booster injection. The study shows that IgE-antibodies to pertussis toxin commonly appear in patients with whooping cough and that the kinetics and the magnitude of the response is influenced by previous exposure to the antigen. A PT-IgE response may also follow pertussis immunization.
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PMID:Immunoglobulin E response to pertussis toxin in whooping cough and after immunization with a whole-cell and an acellular pertussis vaccine. 275 13

Suspended particulate matter (SPM), suspended in the polluted environmental atmosphere, are perpetually inhaled into the human body and are considered to have profound effects on human health. This study investigated the enhancing effect of SPM on the IgE antibody production in mice. The IgE antibody responses in mice immunized with intranasal administration of ovalbumin (OA) plus SPM at 3-week intervals were higher than responses in the animals immunized with OA alone. When the dose of OA administered as an antigen was 0.25 microgram, the time course and magnitude of enhancement by SPM was comparable to those by killed Bordetella pertussis, a common adjuvant. SPM had an enhancing effect on IgE antibody production even in a small dose such as 0.25 microgram administered at 3-week intervals. The possibility cannot be excluded that the natural exposure of humans to SPM in the environmental atmosphere may explain the high prevalence rate of allergic rhinitis caused by pollens in polluted districts in Japan.
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PMID:Enhancing effect of suspended particulate matter on the IgE antibody production in mice. 280 74

Adenosine potentiates mouse bone marrow-derived mast cell mediator release by a mechanism that appears to involve cell surface adenosine receptors. In an attempt to explore possible interactions between G proteins and adenosine receptors, mast cells were incubated with activated pertussis toxin, an agent that ADP-ribosylates and inactivates some G protein subtypes, prior to challenge with specific antigen or the calcium ionophore A23187. Mast cells preincubated with 10 ng/ml pertussis toxin for at least 2 hr exhibited an inhibition of antigen-induced beta-hexosaminidase and leukotriene C4 release. The ability of adenosine to potentiate beta-hexosaminidase release was attenuated to an even greater degree by pertussis toxin. A23187-stimulated mediator release was not altered by pertussis toxin, although a modest inhibition of the ability of adenosine to enhance A23187-induced beta-hexosaminidase release was observed in pertussis toxin-treated mast cells. Although up to 24-hr exposure to 100 ng/ml pertussis toxin did not alter resting mast cell cyclic AMP levels, the ability of adenosine to elevate cell cyclic AMP concentrations was diminished markedly by doses of the toxin higher than those required to affect mediator release. Neither antigen-stimulated intracellular free calcium level augmentation alone nor the additional potentiation of these levels by adenosine was changed by pertussis toxin treatment. Inositol trisphosphate was generated by mast cells stimulated by IgE-mediated mechanisms, but a preincubation with pertussis toxin did not influence its generation. In summary, adenosine appeared to produce some of its alterations in mast cell biochemical events by a mechanism that was partially inhibited by pertussis toxin. The nature of the G protein linked to the mast cell adenosine receptor is yet to be determined.
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PMID:Alteration of mast cell responsiveness to adenosine by pertussis toxin. 284 50

Cooperating with pediatricians in private practice and in hospitals, we tried to evaluate the diagnostic relevance of three serological methods for the detection of antibodies to Bordetella pertussis. The tests employed were a microagglutination, a complement fixation and an enzyme-linked immunoassay (ELISA) to measure specific IgG, IgM, IgA and IgE with whole B. pertussis phase I cells as an antigen. In addition, sera were tested for complement-fixing antibodies to respiratory-syncytial (RS) virus. Microbiological procedures also were used to detect B. pertussis in pernasal swabs. Single sera from 259 children and adults with suspected whooping cough were tested. Of these 117 samples did not contain any measurable antibodies to B. pertussis (45%) and only four sera of this group exhibited complement-fixing antibodies to RS-virus (3%). Antibodies to B. pertussis could be found in the sera of 142 patients. In this group, complement-fixing antibodies to RS-virus were detected in 23 sera (16%). Comparing the methods used to measure antibodies to B. pertussis showed that the ELISA was the most sensitive test, followed by complement fixation and microagglutination. In 21 additional cases, paired sera and several swabs could be obtained from individual patients. These data allowed us to follow the antibody response to B. pertussis during whooping cough, which seemed to be characterized by a relatively late onset with a subsequent rapid increase of initially IgM and IgA and then IgG antibodies. Analogously, the titers of complement-fixing and agglutinating antibodies increased during the later stages of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serological diagnosis of whooping cough. 287 21

High IgE responder rats were sensitized intraperitoneally with alum-adsorbed ovalbumin and Bordetella pertussis organisms. At day 0, 7, 14, 21 and 28 following sensitization the peritoneal cells were harvested and further processed for light and immunoelectron microscopical investigations using a specific anti-rat IgE immunogold sandwich method. The results obtained show that the number of peritoneal mast cells increase significantly during the course of sensitization. There is a time-dependent increase in the amount of immunogold particles on mast cell surfaces together with a shift of particle distribution towards the surface folds. Sensitized mast cells exhibit altered releasability as is indicated by slightly degranulated cells at day 21 and day 28 postsensitization. Additionally, about 25% of small lymphocytes which had entered the peritoneal cavity between day 7 and day 14 are heavily stained with the immunogold complex between day 14 and day 28 postsensitization. This is not so for macrophages (less than or equal to 0.2% positive cells) nor for eosinophils which do not show any staining activity at all despite they are present in high numbers.
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PMID:Time-course of IgE binding to rat peritoneal cells after sensitization with alum-adsorbed ovalbumin and Bordetella pertussis. 288 28

Total IgE and IgG serum levels were measured in rats treated with egg albumin (EA), Bordetella pertussis (Bp) and aluminium hydroxide gel (alum), and in rats administered with Bordetella pertussis or alum alone. Two ELISA micromethods have been developed to measure IgE and IgG changes. Immunoglobulin serum levels were evaluated 14 days after immunization. The highest IgE levels were obtained after sensitization with EA suspended in alum s.c. and administered with Bp i.p. The IgE production induced by Bp alone was significantly lower than that of the former. The IgE concentrations from alum treated group were the same as those obtained in the untreated animals. IgG serum levels remained unchanged in the different immunization procedures assayed.
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PMID:ELISA for total IgE and IgG detection in rat serum. Changes with immunization or adjuvants. 288 32


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