Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0850803 (anaphylaxis)
 8,092 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of leukotrienes and other mediators of vascular changes in anaphylaxis were studied in rats sensitized with monoclonal anti-DNP IgE and challenged with DNP-BSA. Microvascular changes in the mesentery were followed by intravital fluorescent microscopy and in the skin by exudation of Evans blue dye. Administration of Ag i.v. caused a marked increase in the peristaltic movement of the intestine, plasma exudation, and arteriolar constriction in the mesentery. The microvascular changes were accompanied by a profound fall in blood pressure, which was biphasic. The first phase lasted for approximately 2 min. The second phase was very prolonged and the hypotension was still maintained 40 min after Ag challenge. The changes observed were dose dependent with regard to Ag. Intradermal application of Ag resulted in dose-dependent extravasation of Evans blue dye in the skin. Plasma exudation was partially inhibited by pyrilamine and methysergide. However, their effect seemed to be more pronounced in the skin than in the mesentery. The leukotriene D4-R antagonist L-649,923 and the 5-lipoxygenase inhibitor ONO-LP-049, alone or in combination with other inhibitors, did not alter the plasma leakage in the skin. In the mesentery, the leukotriene antagonists alone had a moderate effect on vascular permeability. However, the combination of these agents with pyrilamine completely inhibited macromolecular extravasation. The hypotension was modulated by the antihistamines as well as the leukotriene and serotonin antagonists. Pyrilamine inhibited the first phase and the second phase. The major effect of methysergide was a decrease in the duration of the hypotension. This was especially evident when it was administered in combination with other inhibitors. The leukotriene antagonists when given alone had moderate effects on the blood pressure changes. However, in combination with pyrilamine, the hypotension was substantially reduced. Leukotrienes appeared to be important mediators of the vascular changes in the mesentery but not in the skin (passive cutaneous anaphylaxis). They markedly potentiated the action of histamines.
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PMID:Role of leukotrienes in vascular changes in the rat mesentery and skin in anaphylaxis. 335 3

We tested the effects of pre-treatment with dexamethasone on topically induced ocular anaphylaxis in the rat. Rats were immunized with dinitrophenylated Ascaris suum extract and challenged with di-DNP-lysine. Dexamethasone was administered topically once (24, 6, or 1 h before challenge) or three times (6, 4, and 2 h before challenge). A single pre-treatment given at 24 or 6 h had no significant effect. A single pre-treatment 1 h before challenge reduced the extent of edema assessed histologically but not clinically, and had no significant effect on the eosinophil count in conjunctival tissue examined 6 h after challenge. Eyes pre-treated with dexamethasone 6, 4, and 2 h before challenge showed a significant reduction in conjunctival edema assessed histologically and clinically 1 h after challenge. In addition, 6 h after challenge the number of eosinophils was significantly reduced. We conclude that repeated pre-treatment with dexamethasone can suppress both the immediate phase and the cellular late phase of topically induced ocular anaphylaxis.
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PMID:Effects of topical pre-treatment with dexamethasone on the immediate and late phases of topically induced ocular anaphylaxis in the rat. 336 67

Newborn mongrel dogs were sensitized with conjugates of ovalbumin (OA) and 2,4-dinitrophenol (OA-DNP3) in the presence of Al(OH)3 to produce high levels of anti-OA and anti-DNP IgE antibody. At 4-6 months of age, when anti-DNP and anti-OA antibody levels reached titers of 64 by passive cutaneous anaphylaxis, the dogs underwent separate inhalation and intravenous challenges with conjugates of DNP and bovine gamma globulin (DNP15-BGG) and OA. Inhalation challenge with DNP15-BGG and OA resulted in 5- and 10-fold increases in airflow resistance, respectively. Intravenous challenge with either DNP15-BGG or OA produced profound anaphylaxis with 60-80% decreases in blood pressure, cardiac output and regional blood flows in the carotid, superior mesenteric and renal arteries, and the distal aorta. Treatment of sensitized dogs with 5 doses of 20 mg of conjugates of DNP and polyvinyl alcohol (DNP2-PVA) on alternate days resulted in suppression of anti-DNP IgE antibody production; abrogation of established airway and vascular anaphylactic sensitivities; no change in regional blood flows, and no effect on sensitivities to challenge with OA.
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PMID:A canine model for the study of hapten-specific suppression of IgE-mediated bronchoconstriction and anaphylaxis. 357 May 15

The capacity for IgE anti body production in ASK mice, which are highly sensitivity to anaphylactic shock, was compared with that in C3H and AKR mice. Three strains of mice were immunized with DNP-Ascaris mixed with aluminum hydroxide gel. IgE antibody to DNP in the sera was titrated by the rat 48-hour passive cutaneous anaphylaxis test. Maximum IgE titers of each strain of mice were 1: 2560 in C3H, 1: 1280 in ASK and 1: 640 in AKR. IgE antibody was detected in the sera until 170 days in C3H, 290 days in ASK and for not less than 320 days in AKR. These results suggest that the ASK mouse is a high responder strain for IgE antibody.
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PMID:[Capacity for IgE antibody production in ASK mice]. 406 16

The ability of mouse anti-dinitropheny ovalbumin (anti-DNP-OA) serum to sensitize rat lung fragments can be demonstrated by the release of histamine from the tissue after antigenic challenge. This method can be utilized to evaluate anti-allergic agents, e.g., measuring the inhibition of histamine release by disodium cromoglycate (DSCG). In addition, the method can be utilized to evaluate antibody production, e.g., demonstrating the presence of separate antibodies against hapten and protein carrier in the sera of mice sensitized with DNP-OA. The correlation between heterologous rat passive cutaneous anaphylaxis (HPCA) and pulmonary histamine release for sera was determined by linear regression analysis. The r was greater than 0.8 with 16 observations, suggesting the utility of histamine release as a convenient alternative for pharmacologically evaluating different aspects of the immediate hypersensitivity response.
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PMID:Histamine release from rat lung sensitized in vitro with mouse serum--an alternative pharmacologic method. 615 65

A water-soluble fraction (CEF) obtained from Corynebacterium equi was administered intradermally or intravenously into Sprague-Dawley rats. Passive cutaneous anaphylaxis (PCA) was elicited in these rats along with the controls by sensitization with mouse anti-DNP serum and challenge with the corresponding antigen. PCA reactions were markedly inhibited by the pretreatments of the rats with CEF. Similar treatments of the animals 2-4h after the sensitization did not inhibit PCA. Inhibitory activity of CEF in the pretreated animals was shown to be dose-dependent. Incubation of rat peritoneal mast cells with CEF effectively blocked the binding of murine IgE antibodies to the cells as evidenced by the failure of the treated cells to bind the antibodies. Furthermore, antigen-induced histamine release from rat mast cells, which were sensitized with murine IgE antibodies, was reduced significantly by CEF treatment of the cells prior to the sensitization. Results of this study indicated that CEF inhibits the PCA in rats, presumably by blocking the binding of heterocytotropic antibodies to Fc receptor of mast cells.
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PMID:Regulation of allergic reactions by aerobic Corynebacterium equi extract, CEF. II. Inhibition of Heterologous PCA and antigen-induced histamine release in rats. 617 May 90

Monoclonal DNP-specific IgG (lambda 2 epsilon 2), IgM (kappa 2 mu2) and IgG [kappa 2 (gamma 1)2] were isolated fom the culture supernatant of hybridomas by affinity chromatography with 2,4-dinitrophenol bovine serum albumin (DNP-BSA) sepharose and characterized by biochemical and biological methods. The molecular weights were 84,200 for the epsilon chain, 55,400 for the gamma chain and 77,500 for the mu chain as determined by sodium dodecylsulphate polyacrylamide del electrophoresis (SDS-PAGE). The association constants for [3H]-DNP-lysine determined by equilibrium dialysis were 0 . 87 X 10(7) l/mol for IgE and 1 . 91 X 10(8) 1/mol for IgG1. The isoelectric focusing of the purified monoclonal antibodies revealed for IgG1 seven bands at a pH range of 6 . 3 - 7 . 2 and for IgE sixteen bands at a pH range of 4 . 5 to 6 . 8. the binding of 125I-anti-IgE to rat basophilic leukaemia (RBL) and rat mast cells which had been preincubated with various amounts of monoclonal IgE was studied. At saturation conditions of IgE, about 2 . 14 X 10(5) molecules of anti-IgE were bound per rat mast cell. Rat mast cells coated with monoclonal anti-DNP IgE were triggered for the release of histamine in the presence of either the antigen or guinea-pig anti-mouse IgE. A mutual inhibition of the passive cutaneous anaphylaxis (PCA) reaction in the rat by either mixing mouse reaginic serum directed against ovalbumin or rat reaginic serum directed against Nippostrongylus brasiliensis with monoclonal mouse anti-DNP IgE was demonstrated.
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PMID:Generation of monoclonal murine anti-DNP-IgE, IgM and IgG1 antibodies: biochemical and biological characterization. 618 Sep 75

Two strains of guinea-pigs selectively bred for either high (IMM/S) or low (IMM/R) responsiveness to ovalbumin-induced respiratory anaphylaxis were examined for their immune response to a copolymer of L-glutamic acid and L-alanine (GA), a copolymer of L-glutamic acid and L-tyrosine (GT), and to a dinitro-phenyl derivative of a homopolymer of L-lysine (DNP-PLL). Considerable differences between the strains in development of cellular hypersensitivity and in the production of antibodies were observed. Guinea-pigs from IMM/S were all responders to GA and DNP-PLL and non-responders to GT, while guinea-pigs from two of three lines from IMM/R were responders to GT and non-responders to GA and DNP-PLL. The third IMM/R line showed an immune response pattern similar to guinea-pigs of strain IMM/S. Preliminary breeding studies confirmed that the immune response to these three antigens is under the control of dominant autosomal genes, since (IMM/S x IMM/R) F1 animals responded to all three antigens. It is concluded that these three antigens may serve as immune response markers in genetic studies of the differences between guinea-pigs from IMM/S and IMM/R in their ability to develop respiratory anaphylaxis.
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PMID:Characterization of two strains of selectively bred guinea-pigs. 2. Differences in immune response to synthetic polypeptides. 619 79

The 48-hour passive cutaneous anaphylaxis (PCA) and passive anaphylactic bronchoconstriction in rats induced by an IgE-like antibody against DNP-Ascaris were inhibited by intravenous treatment with traxanox sodium in a dose dependent manner. In both experiments, traxanox sodium was more potent than disodium cromoglycate (DSCG), especially as an inhibitor of bronchial anaphylaxis. In the PCA test of rats using a double sensitization technique according to the Orr's method, traxanox sodium was demonstrated not to inhibit antigen-antibody combination, but to inhibit the release of chemical mediators at a stage following antigen-antibody combination. Traxanox sodium inhibited the complement dependent immune hemolysis, but not the hypotonic hemolysis in vitro. However it failed to inhibit the Forssman anaphylaxis in the guinea pig in vivo. Traxanox sodium (50-250 mg/kg p.o.) showed an inhibitory effect on the direct passive Arthus reaction (DPAR) of the rats. Furthermore, it delayed the onset of the hyperacute form of experimental allergic encephalomyelitis (EAE) and reduced mortality in the rats. DSCG was less effective on DPAR and EAE. In conclusion, traxanox sodium is considered to have a wider spectrum of anti-allergic activity than DSCG since it has a suppressive effect not only on the type I allergic reaction, but also on the type III and IV allergic reactions.
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PMID:[[Effect of traxanox sodium on type I-IV allergic reactions. Studies on anti-allergic agents VII]. 621 52

Antibody contents of IgG1, IgG2a, IgG2b and IgE were measured by enzyme-linked immunosorbent assay (ELISA) in ascites and sera obtained from mice injected with hybridomas producing monoclonal anti-DNP antibodies. In addition, IgG1 and IgE antibodies from sera of immunized mice were also measured by ELISA. Concomitantly, antibody contents were also determined by passive cutaneous anaphylaxis (PCA) in mice for IgG1, IgG2a, IgG2b, by PCA in guinea pigs for IgG2a, by PCA in rats for IgE and by passive hemolysis (PL) for IgG2a and IgG2b. Good correlations were found in the investigated samples between ELISA and the biological determinations.
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PMID:Correlation of murine anti-dinitrophenyl antibody content as determined by ELISA, passive cutaneous anaphylaxis and passive hemolysis. 637 37


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