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)

Preferential enhancement of IgE antibody response was observed in BALF/c mice by the administration of Bordetella pertussis with antigen (DNP-Salmonella). Correlation between B cell mitogenic activity and adjuvant action among B. pertussis, Salmonella, lipopolysaccharide of Escherichia coli and Ficoll was examined but was not found. Thymus-derived cells seemed necessary to develop adjuvant action of B. pertussis since antibody response in athymic nude mice was not influenced by B. pertussis. Helper function of adoptively transfered spleen cells was enhanced by immunization of the donor mice with carrier antigen in the presence of B. pertussis. The magnitude of enhancement was greatest in IgE class. The results indicated that preferential enhancement of IgE antibody formation by B. pertussis is mediated by the augmentation of carrier-specific helper function.
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PMID:Preferential enhancement of IgE antibody formation by Bordetella pertussis. 19 43

Mice exposed to a sublethal dose of X-rays were immunized with alum-precipitated DNP-KLH (dinitrophenyl-keyhole limpet haemocyanin) and B. pertussis either before or after irradiation. The primary anti-DNP antibody response was evaluated during 8 weeks after immunization by the equilibrium dialysis technique using ammonium sulphate- precipitated serum globulins and the ligand 3H-labelled xi-DNP-L-Lysine. The serum concentrations of antibody sites in mice immunized 1-5 days before or 2 h-8 weeks after 450 rad were below the values in unirradiated controls at all bleeding times. Antibody affinity, however, was found to be up to 20 fold higher in irradiated mice than in control mice when antigen was injected before, or 3-8 weeks after, irradiation. Spleen cells from mice exposed to 450 rad 1-9 weeks before killing were stimulated in vitro with PHA, ConA, or LPS. Recovery profiles of mitotic responsiveness suggest that enhancement of antibody affinity in irradiated mice could result from relative lack of suppressor T Cells.
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PMID:Effects of whole-body irradiation on antibody affinity. 19 58

Rats immunized with a purified Ascaris suum allergen (Asc-1) or with its dinitrophenylated derivate (DNP-Asc-1) produced high levels of reaginic (IgE) antibodies. A second injection of antigen given 30 days later did not result in an anamnestic IgE antibody response. Immunization of adult-thymectomized, lethally-irradiated and bone-marrow reconstituted (ATxB) rats with soluble Asc-1 or DNP-Asc-1 failed to stimulate reaginic antibody production. The administration of glutaraldehyde-polymerized antigen induced in some but not all ATxB rats, low but detectable levels of IgE antibodies. These levels increased following a second injection of nonpolymerized antigen in A1 (OH)3 gels. Priming of animals with polymerized carrier and Bordetella pertussis did not stimulate a primary anticarrier IgE response but led to an enhanced antihapten IgE response following the administration of soluble DNP-Asc-1 in A1(OH)3. The results are consistent with the notion that a sharply reduced but clearly functional T-derived helper cell population could be triggered by the polymerized but not by the soluble form of the immunogen.
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PMID:Reaginic antibody production to Ascaris suum allergen, ASC-1. I. The function of glutaraldehyde-polymerized antigen in the induction of reaginic (IgE) antibodies in the rat. 30 62

Although guinea pigs have been frequently used as a model of asthma, antibodies produced in this species are generally gamma1 and gamma2 and belong to IgG. The antibody responsible for asthmatic attacks in humans is IgE, and such is quite different from gamma1 and gamma2, immunologically. Guinea pigs are not therefore an adequate model for investigating anti-asthmatic drugs which inhibit IgE-mediated mediator release, such as disodium cromoglycate. On the other hand, rats do produce an antibody similar to human IgE, the so-called homocytotropic antibody (HTA), by sensitization with dinitrophenylated ascaris extract (DNP-As) together with killed Bordetella pertussis as an adjuvant. To rats actively sensitized with DNP-As or passively sensitized with HTA serum against DNP-As, intravenous administration of antigen did not produce a transient increase in respiration (unlike that of guinea pigs) immediately after the antigen treatment, but a respiratory disorder similar to that seen during asthmatic attacks in humans did occur. The response to antigen was reproducible in passively sensitized rats compared with that of actively sensitized ones, though the symptom was moderate. The effect of N(3', 4'-dimethoxycinnamoyl) anthranilic acid (N-5'), a new anti-allergic drug, was determined in cases of experimental asthma in passively sensitized rats. Respiratory disorders as a result of antigen were clearly inhibited with oral administration of this agent.
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PMID:[Experimental asthma in rats, and the effect of N (3', 4'-dimethoxycinnamoyl) anthranilic acid (N-5') (author's transl)]. 71 Oct 29

The antibody response in mice to DNP-insulin is under Ir-gene control. The Ir gene defects in two strains have been analyzed. In both cases the IgG immune response was impaired whereas the IgM response was not affected. One H-2 gene haplotype was characterized by lack of IgG response, independent of the immunization protocol. A second H-2 haplotype manifested a low response of IgG after immunization with Bordetella pertussis as an adjuvant but a high response after complete Freund's adjuvant. It is proposed that a low level of T cell help induces the production of IgM antibodies, intermediate levels allow few IgG clones to develop, and high levels induce a heterogeneous IgG response.
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PMID:Ir-gene control of antibody class production. 83 64

Neuropeptide Y (NPY) inhibits cardiac adenylate cyclase activity by interacting with specific receptors coupled to a pertussis toxin-sensitive G protein. Structure-activity studies revealed that only C-terminal fragments can exhibit an NPY-like inhibitory effect on 125I-NPY binding and adenylate cyclase activity of rat cardiac ventricular membranes. Although NPY(17-36) inhibited 125I-NPY binding with high potency, it produced a biphasic effect on basal (GTP, 10 and 100 microM or guanosine 5'-gamma-O-(thio)triphosphate (GTP gamma S, 10 microM) adenylate cyclase activity. Low concentrations (less than 1 nM) of NPY(17-36) inhibited the adenylate cyclase activity whereas high concentrations (greater than 1 nM) reversed this action. GTP gamma S (100 microM) reversed the biphasic effect of NPY(17-36). NPY(17-36) exhibited only a stimulatory effect in the membranes from pertussis toxin-treated rats and an inhibitory effect with membranes from cholera toxin-treated rats. Low concentrations (less than 1 nM) of NPY(17-36) inhibited isoproterenol-stimulated adenylate cyclase activity whereas high doses (greater than 1 nM) reversed this activity. The cardiac NPY receptor antagonist, NPY(18-36) (1 microM), completely blocked the biphasic effect of NPY(17-36) on isoproterenol-stimulated activity. The inhibitory dose-response curve of NPY on isoproterenol-stimulated adenylate cyclase activity was shifted parallel to the right by NPY(17-36) (1 microM), suggesting that it is an antagonist of NPY at high concentrations. N-alpha-acetylated and C-terminally deamidated analogs of NPY(17-36) had no effect on the adenylate cyclase activity. [im-DNP-His26] NPY exhibited a more pronounced biphasic effect whereas N-alpha-myristoyl-NPY(17-36) elicited only a stimulatory effect. These investigations suggest that: 1) the inhibitory and stimulatory effects of NPY(17-36) are mediated by high affinity NPY receptors coupled to a pertussis toxin-sensitive G protein and a distinct population of low affinity receptors coupled to a cholera toxin-sensitive G protein, respectively; and 2) the stimulatory effect of NPY(17-36) is dissociable.
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PMID:Inhibitory and stimulatory effects of neuropeptide Y(17-36) on rat cardiac adenylate cyclase activity. Structure-function studies. 153 51

We reported previously that CBA mice pretreated with dinitrophenyl-Bordetella pertussis (DNP-BP) conjugates exhibited sharply decreased anti-DNP IgE, and increased IgG2a antibodies following immunization with DNP-ovalbumin (DNP-OA) in alum. The objective of the present experiments was to determine whether the decrease in anti-DNP IgE was attributed to a regulatory effect exerted by IgG2a antibodies. Anti-DNP monoclonal antibodies (Mab) of the IgG1 or IgG2a isotype were passively transferred to mice, 24 h before a primary immunization with DNP-OA in alum. Anti-DNP IgE production was drastically suppressed in recipients of IgG1 but not of IgG2a Mab. Similar results were obtained when the Mab were endogenously produced by intraperitoneal implantation of anti-DNP-secreting hybridomas into (BALB/cxCBA)F1 (BCF1) mice. However, neither IgG1 nor IgG2a isotypes suppressed IgE antibody production if the hybridoma implantation took place 10 days after hapten priming. These results are, to our knowledge, the first to show a clear dissociation between the effect of either passively transferred or endogenously secreted IgG1 and IgG2a antibodies in their ability to inhibit a primary anti-hapten IgE antibody response.
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PMID:Effect of anti-DNP IgG1- and IgG2a-secreting hybridomas in vivo on the development of an anti-DNP IgE antibody response in mice. 158 6

Brown-Norway rats (male) were sensitized with both dinitrophenylated-bovine serum albumin (DNP-BSA) and Bordetella pertussis simultaneously in order to induce airway hyperresponsiveness (AHR) as the first sensitization. At five days, DNP-BSA was inhaled as a booster into the airways under thiopental anaesthesia. At eight days, inhalation of antigen markedly increased the tracheal pressure (TP) in sensitized rats (11.9 +/- 1.6 cmH2O) and slightly increased TP in non-sensitized rats (1.1 +/- 0.4), the difference between the two groups being significant (p less than 0.001). Twenty-four hours after antigen challenge, the airway responsiveness to ACh in sensitized rats was markedly increased to about 4-fold as compared to that in non-sensitized rats. Inhalation of dinitrophenylated-ovalbumin failed to increase the airway responsiveness to ACh in rats sensitized with DNP-BSA, although a marked increase in TP was induced immediately after antigen challenge. We thus succeeded in preparing a model of AHR by employing a new procedure of sensitization.
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PMID:Induction of airway hyperresponsiveness in allergic rats. 171 32

Extracellular ATP stimulated histamine release and generation of leukotrience C4 (LTC4) accompanied with the formation of inositol phosphates and a rapid increase in intracellular Ca2+ ([Ca2+]i) in mouse bone marrow-derived cultured mast cells (BMMC). The rank order of histamine-releasing potency of ATP and its metabolites is ATP greater than ADP greater than AMP greater than adenosine. Nonhydrolyzable ATP analog, adenosine-5'-O-[2-thiotriphosphate] (ATP-S) released more histamine from the cells than ATP. On the other hand, simultaneous addition of adenosine analogues at micromolar concentrations potentiated histamine release from the cells induced by ATP (50 microM) or DNP-HSA antigen (0.1 ng/ml) in the following rank order: adenosine greater than AMP much greater than ADP = ATP. Histamine release potentiated by adenosine was blocked by the treatment with pertussis toxin, whereas histamine release induced by ATP was not affected by the toxin, suggesting that extracellular ATP stimulate histamine release from BMMC probably via mechanisms independent of the potentiation of histamine release induced by adenosine.
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PMID:The stimuli releasing histamine from murine bone marrow-derived mast cells. 2. Mechanisms involved in histamine release induced by extracellular ATP and its metabolites. 171 46

This report provides a simplified model for investigating the antigen handling mechanisms of the mammalian uterus. The effectiveness of the uterus as a site for systemic immunization has been studied using a hapten-protein conjugate (DNP-BGG) as antigen in nonpregnant virgin rats. The data indicate that although the uterus is inefficient as an antigen delivery site, strong systemic immune responses can be generated under appropriate conditions. Intrauterine (i.u.) immunization with alum-precipitated DNP-BGG did not induce significant antibody activity but primed the females so that vigorous anamnestic responses were produced after a second exposure to (soluble) antigen. The following results were obtained: (1) The optimal immunization dose was 100-2000 micrograms. (2) Alum-precipitation of the immunizing antigen was necessary in order to sensitize the female, while inclusion of killed Bordetella pertussis organisms was not. (3) The site of challenge after i.u. immunization affected the level of serum antibody activity. (4) Retention of antigen within the uterus for as little as 1 day sensitized the females as effectively as 28 days' exposure. (5) The presence or absence of ovarian hormones had no apparent effect in this system.
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PMID:Systemic immunity developing from intrauterine antigen exposure in the nonpregnant rat. 243 Nov 37


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