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Query: UMLS:C0850803 (anaphylaxis)
 8,092 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At least wo histamine receptors have been pharmacologically defined. Using the appropriate agonists and antagonists, the possible involvement of these receptor types in the production of reaginic antibodies in the rodent was investigated. After injecting mice with dinitrophenyl-ovalbumin (DNP-OA), maximal serum reaginic titers occurred on day 11 as measured by heterologous passive cutaneous anaphylaxis. If the mice were dosed daily (i.p.) with the H1 agonist, 2-methylhistamine, or the H2 antagonist, metiamide, the titers of reaginic antibodies on day 11 were significantly higher than the controls. The titers were significantly lower than the controls if an H2 agonist (4-methylhistamine, dimaprit, or impromidine) or if the H1 antagonist, pyrilamine, was administered daily. None of these agents significantly affected total serum IgG titers as measured by ELISA. However, if the mice were injected with DNP-OA on day 0, then dosed daily with metiamide, pyrilamine, or 4 methylhistamine beginning on day 32, the titers of reaginic antibodies elicited by a second injection of DNP-OA given on day 36 were not significantly different from the titers of the non-drug treated mice. Thus, under these conditions, with these agents, the results suggest that histamine receptors may be involved in modulating the production of reaginic antibodies during a primary immunological response, H1 receptor agonists enhanced, while H2 receptor agonists suppressed the responses, and the reverse effect was observed with the appropriate antagonists. However, histamine receptors appear not to be measurably involved in the development of the secondary reaginic response.
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PMID:Effect of histamine agonists and antagonists on the production of murine reaginic antibodies. 646 Jul 5

We established here the experimental asthma model in unanesthetized rat, based on the observation of breathing. The effect of disodium cromoglycate (DSCG) was compared between the passive cutaneous anaphylaxis (PCA) model in rat and our experimental asthma model. The systemic anaphylaxis was elicited, in the rat passively sensitized with reaginic antibodies (reagin) against DNP-As, in response to challenge with antigen. The longer duration of expiration than that of inspiration was observed in the thoracic breathing of antigen-treated rats. The proportion of animals showing this respiratory distress in thoracic breathing (RDTB) was related to the concentration of antiserum used for the sensitization. The relation between RDTB and the concentration of antiserum was more manifest when the degree of RDTB was considered as a score. Inhibition of DSCG was dose-dependent on RDTB and reagin-induced PCA at more than 1 mg/kg. The maximal inhibition of DSCG (20 mg/kg, i.v.) on RDTB or PCA was observed when it was given 30 s before the challenge with antigen. The effect on RDTB decreased gradually with time after dose, and lasted beyond 60 min similar to the inhibitory activity of DSCG on antigen-induced asthmatic reaction in patients. Whereas, the effect on PCA decreased rapidly, and disappeared within 30 min after dose. These results indicate that RDTB is a principal indicator of respiratory distress induced by reagin, and that the effect of DSCG in asthmatics may be explained by its inhibitory activity on RDTB rather than that on PCA.
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PMID:An experimental asthma model in unanesthetized rat, and the difference in effect of disodium cromoglycate between passive cutaneous anaphylaxis model and asthma model in rat. 681 56

After immunization of mice with 2,4-dinitrophenyl-ovalbumin (DNP-OVA), it was shown previously that strains having Igh-Va genes and able to express light chains of the Vk1 group produce high levels of anti-DNP antibody bearing an idiotype (Id-460) associated with the combining site of the BALB/c DNP-binding myeloma protein MOPC 460. Expression of Id-460 in serum is transient; Id-460 levels peak early in the response and are regulated independently of total anti-DNP antibody. In this paper, the transient dominance of Id-460 expression has been confirmed at the cellular level by inhibition of splenic anti-DNP plaque-forming cells (PFC) with rabbit anti-Id-460 antiserum. Id-460+ PFC can account for 52-91% of anti-DNP PFC early after secondary challenge with DNP-OVA. Furthermore, Id-460 is represented at these high levels in IgM, IgG, and IgG1, and IgG2a, the three isotypes tested in the PFC assay, as well as in IgE, as tested by passive cutaneous anaphylaxis. Thus, there is no preferential association of Id-460 with a given isotype. We conclude from these studies that Id-460 is a dominant idiotype in the anti-DNP antibody response of BALB/c mice to DNP-OVA. This dominance is expressed transiently and is independent of isotype. A further conclusion from these studies is that regulation of isotype expression is independent of the regulation of idiotype expression in this system. We would suggest that regulation of Id-460 expression involves Ig-dependent helper T cells specific for Id-460 that induce Id-460+ B cells and also activate suppressor T cells, both events occurring via idiotype-anti-idiotype interactions.
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PMID:Expression of an idiotype (Id-460) during in vivo anti-dinitrophenyl antibody responses. II. Transient idiotypic dominance. 702 12

A method was developed to induce contraction of immunologically sensitized mouse trachea by antigen (Schultz-Dale reaction). The response was mediated by immunoglobulin (Ig) E antibody directed against either the hapten DNP, the hapten carrier conjugate DNP-keyhole limpet hemocyanin (KLH), or the unmodified carrier KLH. Tracheal contractions were elicited by DNP-KLH, KLH, or DNP-bovine serum albumin (BSA) but not by DNP or BSA alone. This procedure represents a useful index of in vitro anaphylaxis in mouse airway smooth muscle.
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PMID:Schultz-Dale reaction in mouse trachea. 726 92

With regard to our studies on the functional properties of bovine IgG1 and IgG2 antibodies, the differences were minimal when homologous systems were evaluated. Both IgG1 and IgG2 fixed bovine complement by the classical pathway, caused homologous passive cutaneous anaphylaxis, caused phagocytosis of coated erythrocytes by cultured monocytes and precipitated with an antigen having multiple unique determinants (ovalbumin). In contrast to IgG2, IgG1 caused neither adherence nor phagocytosis by freshly isolated neutrophils and monocytes. Additionally, IgG2 antibodies to DNP precipitated with DNP19ovalbumin while IgG1 antibodies formed soluble complexes with this antigen.
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PMID:Biologic activities of bovine IgG subclasses. 733 44

The IgE antibody responses of inbred BALB/c mice to subcutaneously injected antigens, given without adjuvant, were studied. Cocksfoot grass pollen extract (GPE) (100-100,000 pnu) induced no detectable primary IgE antibody responses but following second and subsequent injections, substantial secondary responses were produced. Weekly injections for 9 weeks of doses of doses of 0.1-10,000 pnu GPE all produced similar IgE antibody titres as measured by 24 h passive cutaneous anaphylaxis (PCA) in rats challenged with 16,000 pnu GPE. A similar schedule of injections of doses of 10(-10)-10(-5) g of DNP-OA also produced substantial and similar anti-DNP IgE antibody titres as measured by PCA in rats challenged with 1 mg DNP-BSA. As the challenging dose of DNP-BSA used in the induction of PCA was reduced progressively however, the PCA titres of the mouse sera showed more and more dependence on immunizing antigen dose. At limiting doses of antigen in PCA, the serum titres rose to a peak and then declined, as the immunizing dose of DNP-OA used in the mice was progressively increased. The possible implications of these results with regard to our understanding of the IgE antibody response in atopic patients is discussed.
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PMID:Ige antibody formation in BALB/c mice without adjuvant: induction of responses to grass pollen extract and to a hapten-carrier conjugate. 738 Apr 80

The effect of histamine on nasal mucosal permeability against an antigen was investigated by using modified passive cutaneous anaphylaxis (PCA) reactions in normal and actively sensitized guinea pigs. The administration of a dinitrophenyl-coupled Ascaris (DNP-Ascaris) solution as an antigen into the nasal cavity caused PCA reactions in the dorsal skin of normal guinea pigs. The administration of histamine into the nasal cavity before the antigen treatment significantly enhanced the anaphylactic responses. The PCA reactions did not occur when ovalbumin (OA) was administered intranasally in normal guinea pigs. In guinea pigs sensitized against DNP-Ascaris, however, PCA reactions to anti-OA antiserum were elicited by the intranasal administration of OA. The intranasal administration of histamine before the antigen treatment also enhanced anaphylactic responses in sensitized guinea pigs. These results indicate that histamine increases nasal mucosal permeability and that this may be one of the causes of nasal hypersensitivity in nasal allergy.
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PMID:Ability of histamine to increase nasal mucosal permeability to macromolecules in guinea pigs. 749 70

In this study we established that the conjugate of ovalbumin (OVA), which was used as a model allergen, with monomethoxypolyethylene glycol (mPEG), i.e., OVA(mPEG)11, was not only tolerogenic and essentially non-allergenic, but also capable of inactivating mast cells sensitized with anti-OVA IgE antibodies (Abs). Moreover, mast cells sensitized with a mixture of anti-OVA and anti-DNP IgE Abs were also desensitized by OVA(mPEG)11 with respect to both sensitivities. Most importantly, treatment of OVA-sensitive mice by OVA(mPEG)11 protected them from systemic anaphylaxis on challenge with OVA. The possibility of inactivating IgE-sensitized mast cells with mPEG conjugates of single epitopes of a given allergen is being investigated.
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PMID:Inhibition of the effector phase of IgE-mediated allergies by tolerogenic conjugates of allergens and monomethoxypolyethylene glycol. 761 57

Xian-Qing-Long-Tang (XQLT), a Chinese medicine, is useful for treating allergic diseases. To demonstrate the anti-allergic effect of this drug we examined its effect on degranulation and histamine release from rat mast cells induced by antigen and compound 48/80. The effect on 48 h homologous passive cutaneous anaphylaxis (PCA) in rats was also studied. In the IgE antigen-antibody reaction using DNP-As, XQLT inhibited histamine release from rat mast cells, in vitro; it also inhibited 48 h rat homologous PCA reaction, in vivo. These results suggest that XQLT inhibits type 1 allergic reaction, and has effectiveness for allergic disease.
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PMID:Inhibitory effect of xian-qing-long-tan extract on degranulation and histamine release from rat mast cells. 768 May 18

Cross-linking of the high affinity IgE receptor (Fc epsilon RI) expressed on mast cells and basophils is essential for triggering anaphylaxis in vivo. Previously, other investigators have tried to produce competitive inhibitors using IgE peptide analogues and anti-IgE antibodies with limited success. To create a novel specific inhibitor of IgE that can block binding of IgE to Fc epsilon RI without the capacity to stimulate degranulation, we made an Fc epsilon RI-IgG immunoadhesin. The Fc epsilon RI-IgG was constructed by gene fusion of the extracellular portion of the human alpha-chain of Fc epsilon RI, which contains the high affinity binding site for IgE, with a truncated human IgG1 H chain C region. The Fc epsilon RI-IgG recognizes both human and murine IgE. Coincubation of Fc epsilon RI-IgG with murine IgE prevented sensitization of RBL-2H3 cells and the subsequent histamine release in response to anti-IgE. Similarly, when the Fc epsilon RI-IgG was preincubated with equimolar concentrations of either hyperimmune mouse sera or purified mouse IgE, it completely blocked the passive cutaneous anaphylaxis reaction in rats. Furthermore, i.v. administration of Fc epsilon RI-IgG following intracutaneous injection of serum from DNP-immunized mice was able to block the passive cutaneous anaphylaxis reaction in a time-dependent fashion. These results demonstrate that Fc epsilon RI-IgG is a potent inhibitor of IgE binding to intracutaneous mast cells in vivo and may prove clinically useful for the treatment of IgE-mediated disease.
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PMID:Human IgE receptor alpha-chain IgG chimera blocks passive cutaneous anaphylaxis reaction in vivo. 768 40


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