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Results for “Passive Cutaneous Anaphylaxis”

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At least 19 recordsLinked to original sources

An ELISA-based method for measurement of food-specific IgE antibody in mouse serum: an alternative to the passive cutaneous anaphylaxis assay.

Passive cutaneous anaphylaxis (PCA) assay has been a gold standard method to measure allergen-specific IgE antibody (ASIgE Ab) levels in allergy mouse models. Many factors including stringent guidelines for laboratory animal use make PCA a difficult choice. Therefore, alternative methods are needed that can be readily applied for measurement of specific IgE antibody levels in mouse serum. Herein we describe a novel ELISA-based method that is more sensitive in comparison to PCA, IgE isotype-specific (because it has little cross-reactivity with IgG1 or IgG2a isotype) and highly reproducible (<10% inter- or intra-assay variation). Furthermore, we demonstrate the utility of this assay to measure specific IgE Ab against a variety of food extracts including chicken egg, peanut, almond, filbert/hazelnut and sweet potato. These findings are of particular interest to those who are seeking (i) to measure food-extract-specific IgE antibody in animal models and (ii) an alternative to the animal-based PCA method to measure mouse IgE antibodies.

Allergens↗

The effects of H1 and H2 receptor antagonism on the response of monkey skin to intradermal histamine, reverse-type anaphylaxis, and passive cutaneous anaphylaxis.

The effects of H1 and H2 receptor anatagonists on models of allergic reactions in monkey skin have been studied. Intradermal histamine is markedly inhibited by H1 receptor antagonists but not by H2 receptor antagonists in the doses used. However, the combination of both receptor antagonists gives greater inhibition than that seen with H1 receptor blockade alone. Reverse-type anaphylaxis is also markedly inhibited by H1 but not H2 receptor antagonists. Passive cutaneous anaphylaxis (PCA) is likewise inhibited by H1 receptor antagonism, but not by H2 receptor antagonism. The combination of the two inhibitors leads to a complete inhibition of this PCA response. The data suggest that the addition of an H2 receptor antagonist may potentiate the effect of H1 blockade alone.

Anaphylaxis↗

Correlation of murine anti-dinitrophenyl antibody content as determined by ELISA, passive cutaneous anaphylaxis and passive hemolysis.

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.

Animals↗

ELECTROPHORETIC SEPARATION AND PROPERTIES OF MOUSE ANTIHAPTEN ANTIBODIES INVOLVED IN PASSIVE CUTANEOUS ANAPHYLAXIS AND PASSIVE HEMOLYSIS.

Some properties of mouse antibodies produced by hyperimmunization with conjugated haptens, emulsified in complete adjuvant, have been investigated. Under these conditions two antigenically different types of precipitating antibody, with small differences in their electrophoretic mobilities, both migrating in the gamma-region, are produced. Both antibody types were shown to be different from the beta(2A)-globulins) as revealed by the absence of reaction with specific rabbit antisera against mouse beta(2A)-myeloma globulins. gamma(2) or the slower migrating antibodies, similarly to what has been described for the guinea pig, were able to provoke lysis of antigen-coated tanned sheep erythrocytes, in the presence of complement. This activity could not be detected in the faster migrating antibody type. The slower migrating fractions of the gamma(2)-antibodies were able to transfer passive cutaneous anaphylaxis (PCA) in the guinea pig, but not in their own species. gamma(1)-Antibodies were found to be capable of sensitizing the mouse for cutaneous anaphylaxis. The sensitivity of these antibodies to reduction and alkylation was different, the lytic activity being practically abolished, the PCA titers in mice much reduced, and the PCA activity in guinea pigs only partially inactivated.

Animals↗

Rat monoclonal anti-murine IgE antibody removes IgE molecules already bound to mast cells or basophilic leukemia cells, resulting in the inhibition of systemic anaphylaxis and passive cutaneous anaphylaxis.

IgE plays a central role in allergic reactions. Some anti-IgE antibodies (HMK-12, 6HD5) inhibit the binding of IgE to the FcepsilonRI of mast cells/basophilic leukemia cells (PT-18, RBL/2H3), but less inhibition is seen with the anti-allotypic JKS-6 and the anti-idiotypic Eb-1. Anti-IgE HMK-12 can detach bound IgE molecules from the FcepsilonRI. When mast cells or basophils were incubated with monoclonal anti-DNP-IgE SPE-7, washed and treated with anti-IgE HMK-12, anti-IgE/IgE complexes were found in the supernatant. Similar results were obtained with the Fab fragment of HMK-12. Mice injected with anti-DNP-IgE SPE-7 and later with DNP-BSA had the typical systemic anaphylactic shock. However, if they were injected with the anti-IgE antibody (HMK-12) before the challenge, they did not get an anaphylactic shock. In the sera of mice injected with monoclonal IgE SPE-7 and anti-IgE antibody (HMK-12), IgE/anti-IgE complexes were detected. No passive cutaneous anaphylaxis occurred if the rats were injected with anti-IgE antibodies before the challenge. In summary, anti-IgE antibodies can remove IgE antibodies from the FcepsilonRI; anti-IgE/IgE complexes can be detected in vitro and in vivo, and anti-IgE antibodies can inhibit IgE-mediated systemic or local anaphylactic reactions.

Anaphylaxis↗

Suppression by mepyramine maleate of the increased vascular permeability in passive cutaneous anaphylaxis in the chicken.

Passive cutaneous anaphylaxis was produced in chickens pretreated with the antihistamine mepyramine maleate. Quantitative estimation of the increased vascular permeability in the lesion revealed 79.5% suppression indicating its mediation largely by histamine. The findings suggest that the quantitative estimation of the increased vascular permeability, though time-consuming, is more precise than the visual assessment.

Aminopyridines↗

A topographical study of increased vascular permeability in passive cutaneous anaphylaxis in the chicken.

Passive cutaneous anaphylaxis was produced in chickens with bovine serum albumin (BSA) and anti-BSA chicken serum. Colloidal carbon was then given intravenously to identify the leaky vessels. Microscopic examination of cleared unstained skin revealed the topography of labelled vessels. The carbon labelling was confined to venules and small veins only. Examination of the time-course of permeability response revealed a biphasic pattern.

Animals↗

A microscopic study of increased vascular permeability and leucocyte emigration in passive cutaneous anaphylaxis in the chicken.

Passive cutaneous anaphylaxis was produced in chickens with bovine serum albumin (BSA) and anti-BSA chicken serum. Colloidal carbon was then given intravenously to identify the leaky vessels. Examination of the resulting sequential changes revealed a marked increase in vascular permeability affecting the venules. A noteworthy feature of the reaction was the early participation of the basophils, which contained phagocytosed carbon particles. Eosinophils were absent.

Animals↗

Sensitivity of passive cutaneous anaphylaxis in rats. II. Suppression of passive cutaneous anaphylactic reactions in rats infected with Nippostrongylus brasiliensis.

The sensitivity of passive cutaneous anaphylactic (PCA) reaction was examined in rats infected with the nematode parasite, Nippostrongylus brasiliensis (Nb). PCA reactions with anti-DNP IgE antibody were remarkably suppressed by Nb infection already 10 days after infection and persisted for at least 28 weeks. 10 days after infection, no anti-Nb IgE antibody was present in the sera of infected rats, whereas 18 or 28 weeks after infection, circulating anti-Nb IgE antibody was present. It was concluded that two different mechanisms might explain the suppression. 10 days after infection, nonspecific IgE induced by potentiated IgE production inhibited passive sensitization with anti-DNP IgE antibody by occupying the IgE receptors on mast cells, whereas 18 or 28 weeks after infection, the mast cell IgE receptors were occupied by IgE antibody specific for the Nb antigen. The reactivity through non-immunological processes (skin sensitivity to compound 48/80) was not modified by Nb infection at any time after infection.

Animals↗

Passive cutaneous anaphylaxis in the domestic fowl.

Passive cutaneous anaphylaxis (PCA) has been demonstrated in young and adult domestic fowl using antisera obtained from actively sensitized chickens on the day of their maximal susceptibility to systemic anaphylaxis. Young chickens are more sensitive to histamine and PCA reaction than adults. The PCA reaction was inhibited by the H1-histamine receptor blocker, mepyramine. In the PCA reaction of 2 h sensitization period, the main exudating cells were heterophils, mononuclear cells (lymphocytes, monocytes and macrophages) and some basophils. This study suggests a possible role for circulating basophils in the mediation of early acute inflammatory reaction of immunological origin.

Aging↗

Readministration of IgE is required for repeated passive cutaneous anaphylaxis in mice.

BACKGROUND: Homologous passive cutaneous anaphylaxis (PCA) is an established technique that provides a useful tool to study local inflammation due to mast cell activation. Since mast cells are responsive to repeated challenge by IgE receptor crosslinking in vitro, we investigated the responsiveness of mice to repeated PCA activation. METHODS: Female BALB/c mice were sensitized with intradermal injection of IgE into the ear and provocated through intravenous injection of trinitrophenol-BSA. Repeated provocation was administered, and the outcome was determined by colorimetrical measurement of Evans blue dye leakage. RESULTS: After local IgE injection, mice could be challenged to demonstrate a PCA reaction at least up to 13 days after IgE sensitization. In contrast, passively sensitized mice did not respond to repeated antigen challenge, i.e. a second provocation administered between 1 and 12 days after the first PCA reaction. However, if these mice were intradermally resensitized with IgE at the same site after the first challenge, they became responsive to the repeated challenge. CONCLUSIONS: Mast cells become desensitized upon PCA reaction, and resensitization with IgE is critical for mice repeatedly stimulated by PCA activation.

Animals↗

Biphasic response of cutaneous blood flow induced by passive cutaneous anaphylaxis in rats.

In the immediate phase of passive cutaneous anaphylaxis, sensitized skin mast cells release various mediators when activated by antigen. The present study investigated the effects of the mediators on cutaneous blood flow at the antigen-antibody reaction site. Induction of passive cutaneous anaphylaxis produced a biphasic response consisting of an initial decrease, followed by a sustained increase, in the cutaneous blood flow. The initial phase was almost eliminated by the 5-hydroxytryptamine receptor antagonist methysergide, whereas the second phase was sensitive to the histamine H(2) receptor antagonist ranitidine. The histamine H(1) receptor antagonist chlorpheniramine, the denervation of sensory nerves with capsaicin, the cyclooxygenase inhibitor indomethacin, or the bradykinin B(2) receptor antagonist D-arginyl-L-arginyl-L-prolyl-trans-4-hydroxy-L-prolylglycyl-3-(2-thienyl)-L-alanyl-L-seryl-D-1,2,3,4-tetrahydro-3-isoquinolinecarbonyl-L-(2alpha,3beta,7abeta)-octahydro-1H-indole-2-carbonyl-L-arginine (HOE140) did not affect the blood-flow changes caused by the anaphylaxis. These results suggest that 5-hydroxytryptamine and histamine H(2) receptors mediate the initial decrease and the subsequent increase in cutaneous blood flow, respectively, induced by passive cutaneous anaphylaxis in rats.

Animals↗

[Mediator release assay of rat basophil leukemia cells as alternative for passive cutaneous anaphylaxis testing (PCA) in laboratory animals].

Passive cutaneous anaphylaxis (PCA) is an animal model for inflammatory reactions in Type I allergy. An in vitro assay based on IgE dependent and allergen-induced mediator release of RBL-2H3 cells is presented as an alternative for PCA. The assay has been adopted to the special needs of examining allergen extracts and has been proven to be practicable and reliable. A high number of samples can be processed quickly in one assay, with intra-assay variations below 10%. The first successful applications are the measurement of biologic potencies in allergenic extracts and the determination of murine serum IgE antibodies. Further studies will show whether this assay is suited to evaluate the efficiency of anti-inflammatory and anti-allergic drugs.

Allergens↗

Homologous passive cutaneous anaphylaxis in various strains of mice.

Passive cutaneous anaphylaxis (PCA) was elicited both in the ear and in the dorsal skin of 13 strains of mice at the same time and assessed quantitatively by measuring the amount of extravasated dye. Body pigments of colored mice such as DBA/2 (chocolate), C3H/He (brown) and C57BL/6 (black) did not interfere with the measurement of dye. In the ear response, ICR was a higher responder, C57BL/6 and BALB/c-nu/nu were lower responder strains. In the dorsal skin response, however, ICR was a lower responder, BALB/c-nu/nu, Hairless and WBB6F1-+/+ were higher responders. WBB6 F1-W/Wv was a nonresponder in both responses. The ear response was highly reproducible and the dorsal skin response of each strain was 1/2-1/10 of its ear response except for BALB/c-nu/nu. The PCA bluing regions on the dorsal skin of BALB/c-nu/nu were clearly delineated and the response was almost comparable to its ear response.

Animals↗

[Induction of passive cutaneous anaphylaxis by oral administration of antigen].

Passive cutaneous anaphylaxis (PCA) reaction was developed by Ovary et al. as an animal model of mainly human type I allergic inflammation reaction. This is the most sensitive reaction for the detection of cutaneously sensitizing antibodies and provides a very effective means by which to investigate immunological reactions concerning the mechanisms of development and inhibition of allergic reactions, levels and specificity of antibodies, and the structure of antigens. These cutaneous inflammations mimic atopic dermatitis. Food ingestion has been pointed out as one of the worsened factors of atopic dermatitis. However, the body is generally protected against the invasion of high molecular substances such as non-ingested food by several barriers including digestive enzymes that break down complex food molecules into simpler substances and gastrointestinal mucosae. Accordingly, oral ingestion of food antigen seems to be physiologically and immunologically in conflict with the occurrence of dermatitis. With a view to determining whether allergic dermatitis occurs after oral ingestion of food, the present study was carried out on animals, utilizing the PCA reaction. C 57 BL/6 Ncr j mice were immunized with immunogen derived from commercially obtained eggs. Wistar rats were used as a model of PCA reaction. The results of the present investigation are summarized as follows. 1) Blue spots of 10 mm diameter were observed as a PCA reaction 50 min or more after oral administration of antigen, and the blue spots reached maximum size (20-21 mm, 1.8-1.7 micrograms) after 90-120 min. The PCA reaction was induced 20 min or more after intravenous administration of antigen. When the maximum reaction was compared between the oral and the intravenous routes after 50 min (29.5 micrograms) and 90 min (1.8 micrograms) respectively, there was about a 16-fold difference in the capacity to induce inflammations. 2) The maximum PCA reaction values were 100 and 1,600 for the oral and intravenous routes, respectively, there being a 16-fold difference between the two routes. 3) The minimum antigen concentration required to induce the PCA reaction was 10 mg/ ml for the oral route and 0.01 mg/ml for the intravenous, there being a 1,000-fold difference between the two routes. 4) Reactions with anti-egg mixture antibody and main egg constituents were specific. The PCA inhibition test results confirmed that the undigested structural portion of antigen was associated with the induction of PCA. The present investigation demonstrated that there existed a mechanism by which type I allergy is induced via the gastro-intestinal tract. This fact indicates that part of the food ingested undergoes no change in its molecular structure when transferred to the blood, thus acting as a PCA inducing antigen. This phenomenon suggests that this animal model of human type I allergic dermatitis is a useful system that strongly suggests the association of food antigen with the development of allergic dermatitis.

Administration, Oral↗

Passive cutaneous anaphylaxis with antigens from Coxiella burneti.

Passive cutaneous anaphylaxis (PCA) was produced in guinea pigs sensitized with guinea pig Coxiella burneti phase I-II antiserum and challenged with dimethylsulfoxide- or trichloroacetic acid-soluble extracts from phase I cells. The PCA reaction could not be induced by whole or mechanically disrupted phase I or phase II C. burneti cells or by extracted cells or extracts of phase II cells. The antibody responsible for PCA was in the 7Sgamma(1) (fast gamma) globulin. Sensitization of the skin by 7Sgamma(1) antibody could be blocked nonspecifically by 7Sgamma(1) globulin from normal serum or from phase II antiserum. The 7Sgamma(2) (slow gamma) globulin antibody inhibited the reaction specifically. Some antiserum pools containing high agglutinin and complement-fixing titers to phase I C. burneti cells failed to initiate the PCA reaction, perhaps due to an imbalanced ratio of gamma(1) to gamma(2) specific globulins or to an imbalance in the ratio of specific to nonspecific gamma(1) globulins. Agglutinins to phase I cells were found in both gamma(1) and gamma(2) antibody globulins. Complement-fixing antibodies were found in the gamma(2) globulin fraction.

Agglutination Tests↗