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Results for “Passive Cutaneous Anaphylaxis”

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At least 19 recordsLinked to original sources
PubMed1979

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↗
PubMed1977

Role of mouse IgG and IgE homocytotropic antibodies in passive cutaneous anaphylaxis.

The role of the mouse homocytotropic antibodies in passive cutaneous anaphylaxis reaction was investigated. One class of antibody was heat stable, detected at 2 h but not at 48 h after passive transfer, and belonged to a sublcass of mouse IgG. The other was heat labile, detected at 2 h and 48 h after passive transfer, and belonged to the IgE class of mouse immunoglobulins. In the presence of IgG, IgE homocytotropic antibody was not detected early after passive transfer. This was thought to be due to a masking of IgE by IgG antibodies rather than a competition for mast cell surface receptors, since inhibition studies with rat IgE myeloma protein suggested that mouse IgE and IgG1 may have different receptor sites on mast cell surfaces.

Animals↗
PubMed1975

Antibody-mediated and delayed-type hypersensitivity reactions to Brucella skin test antigens in guinea pigs.

Cutaneous hypersensitivity responses to brucella antigens of different composition were studied in guinea pigs sensitized by infection with smooth brucella or immunization with killed rough brucella in adjuvant. These animals had circulating antibodies to smooth lipopolysaccharide or protein antigens, respectively. Intradermal skin tests, active cutaneous anaphylaxis, passive cutaneous anaphylaxis, and immunodiffusion tests were performed. Delayed-type hypersensitivity reactions uncomplicated by accompanying antibody-mediated reactions were seen only in infected guinea pigs with protein antigen that was entirely free of lipopolysaccharide. In the adjuvant-immunized animals, the protein antigen evoked overlapping antibody-mediated and delayed-type reactions. Lipopolysaccharide and polysaccharide preparations contained varying amounts of protein components. In infected animals, reactions of these antigens were clearly antibody mediated, but participation of delayed-type hypersensitivity could not be excluded. In adjuvant-immunized animals, the antibody-mediated reaction to the lipopolysaccharide preparation was caused by its protein component.

Animals↗
PubMed1975

Local effect of single stranded polyadenylic acid on passive cutaneous anaphylaxis in mice.

Single stranded polyadenylic acid (Poly A) administered locally inhibited passive cutaneous anaphylaxis in mice. In experiments performed by equilibrium dialysis Poly A was able to bind histamine. The association constant of the reaction was determined, Ka = 1.3 +/- 0.2 x 10(5) I/M. One Poly A molecule can bind maximally two molecules of histamine dichloride. Poly A inhibited the antigen-induced release of histamine from the peritoneal rat mast cells when it was given together with sensitizing antibodies.

Animals↗
PubMed1978

Inhibition of allergic reactions by a new antiallergic drug, LC-6 (trans-2,3b,4,5,7,8b,9,10-octahydronaphthol[1,2-c:5,6-c'] dipyrazole). I. Inhibition of the rat reaginic passive cutaneous anaphylaxis.

A new synthetic compound, LC-6, has been shown to inhibit the passive cutaneous anaphylaxis reactions induced in rats by mouse reaginic antibody. In this system, the ED50 was 35 mg/kg body weight of LC-6 administered per os. LC-6 prevented neither histamine skin reactions nor the reactions to histamine and other chemical mediators released by 48/80. Therefore, its inhibitory activity is comparable to that of the model anti-allergic compound, disodium cromoglycate (DSCG). In contrast to DSCG, the new drug exhibits the distinct advantage of being active per os and over prolonged periods of time. Its activity has been shown to persist for at least 6 h when doses 4 times higher than the ED50 were administered. The duration of the drug effect was clearly dose-dependent. Predoses of the compound increased its effectiveness. The long-lasting association of LC-6 with mast cells, as indicated by its prolonged inhibitory activity, makes it a valuable tool in the search for receptors involved in anaphylactic reactions.

Animals↗
PubMed1978

Quantitation of passive cutaneous anaphylaxis (PCA) by using radiolabelled antigen.

The major problem of detecting reaginic antibody by passive cutaneous anaphylaxis (PCA) is the quantitation of the dye reaction. Radiolabelled antigen was used in an attempt to quantitate the PCA reaction (Radio-PCA). Antisera containing reaginic antibody against human serum albumin (HSA) were produced in rabbits. These antisera were injected into normal rabbit skin in different dilutions. Twenty-four hours later HSA was injected intravenously either with Evans Blue or as 125-I-HSA. Radioactivity found in antibody-containing skin was significantly higher than in control specimens containing saline or normal rabbit serum, as low as antiserum dilutions of 1:1,000. Compared with the Evans Blue technique Radio-PCA was able to distinguish quantitatively between different antiserum dilutions at a higher level of statistical significance.

Animals↗
PubMed1977

Effect of Trichinella spiralis infection on passive cutaneous anaphylaxis in mice.

Infection of CFW mice with Trichinella spiralis induced a state of relative unresponsiveness to passive cutaneous anaphylaxis (PCA) induced with hen egg albumin and its corresponding antibodies. The unresponsiveness was to PCA produced either with immunoglobulin G1 (IgG1) or IgE type of antibodies, but was more pronounced with the latter. As few as 25 larvae given by stomach tube 20 days before induced this resistance, although 400 larvae induced a greater resistance. When 400 to 600 larvae were fed to mice, the refractoriness of these mice to PCA was noticed 15 days later. The sera of infected mice had the ability to inhibit mainly PCA induced by IgE. This inhibitory property of sera from infected mice was more pronounced 35 days after infection than 10 months later, when only weak inhibitory activity was detected. Purified rat IgE inhibited the PCA reactions induced in both mice and rats with mouse IgE-type antibody. At high concentrations, evidence of inhibition of the IgG1-induced PCA in mice was also obtained. We believe that the relative unresponsiveness of infected mice is due to an increase in production of IgE which competitively blocks the mast cell sites for other IgE molecules.

Animals↗
PubMedDate not supplied

Passive cutaneous anaphylaxis: improvement of quantitative analysis by radioactively labelled antigen.

Experiments were performed to improve the quantitative analysis of passive cutaneous anaphylaxis (PCA) by labelling the antigen with radioactive iodine. After intradermal injection of antibodies and intravenous administration of labelled antigen in rats a close correlation was found between the radioactivity measured in skin biopsies and the amount of antigen as well as the amount of antibodies. This direct dependence makes it possible to improve quantitatively the reading of PCA test results. A quantitative correlation was also found when radioactivity is measured over the skin by scanning procedures. Therefore it is not necessary to cut out skin biopsies. Thus the same test animal can be used several times, which minimizes biological variations.

Animals↗
PubMed1978

[Pharmacological properties of N-(3',4'-dimethoxycinnamoyl) anthranilic acid (N-5'), a new anti-atopic agent. (3).--Influence on homologous passive cutaneous anaphylaxis mediated by homocytotropic antibody (author's transl)].

N-5' shows a potent inhibitory action on the homologous passive cutaneous anaphylaxis (PCA) in rats mainly through the inhibition of histamine release from mast cells. The present experiment was an attempt to clarify in detail the pharmacological properties of N-5'. Inhibition of PCA was most potent at 30 or 60 min pretreatment with N-5', and negligible at 240 min pretreatment. Given p.o., N-5' produced a dose-dependent, potent inhibitory action at 30-min pretreatment. On the other hand, disodium cromoglycate (DSCG) had little effect on PCA when given orally. On the case of i.v. administration, N-5' (20 mg/kg) and DSCG (5 mg/kg) showed a most potent inhibition of PCA at 5 min pretreatment. The inhibitory action of DSCG was, however, shorter lasting than that of N-5'. Median effective doses (ED50) of DSCG and N-5' on the PCA were estimated to be 0.79 and 8.8 mg/kg i.v., respectively. Inhibitory activity of N-5' in the adrenalectomized rat did not differ from that in sham operated animals. N-5' had a more potent inhibitory action on the PCA in infant rats than in adults. Inhibitory activity of N-5' in the case of 1, 2, 3 and 4 weeks of successive administration was equipotent to that with a single administration.

Administration, Oral↗
PubMed1975

An analysis of the specificity in pharmacological inhibition of the passive cutaneous anaphylaxis reaction in mice and rats.

An antiserum obtained from mice, immunized to produce an antiovalbumin antibody of the IgE type, was employed in a 48-hour passive cutaneous anaphylaxis (PCA) reaction in both mice and rats. The antiserum contained an antibody which, "fixed" to skin for at least 6 days, was heat labile and eluted from diethylaminoethyl cellulose in the reagin peak. In both rats and mice, the PCA reaction was mediated by a combination of histamine and serotonin and was inhibited by specific antagonists. Various drugs were tested for inhibition of the PCA reaction in recipients also injected with compound 48/80 and histamine. Drugs which have been reported to cause an increase in intracellular cyclic adenosine monophosphate levels [prostaglandins (PG) E1 and E2 and theophylline] all selectively inhibited the PCA reaction at low doses. By varying the length of time of drug administration prior to antigen challenge, the pharmacological half-life of PGE1 was determined to be approximately 9 minutes. At high doses, theophylline also inhibited the 48/80 reaction, and PGE1 inhibited all three reactions, whereas PGE2 only inhibited PCA. Disodium cromoglycate, when given to rats, inhibited only the PCA reaction without effect on the 48/80 or histamine wheal. It was totally ineffective on any parameter measured in the mouse. It is suggested that the PCA reaction in the rodent is induced by an IgE-like antibody and mediator release is, to some extent, sensitive to intracellular levels of cyclic adenosine monophosphate. Analysis of the specificity of drug activity depends upon dose-response studies, species differences and consideration of nonspecific systemic effects.

Animals↗
PubMed1979

A new method of allergen standardization. Passive cutaneous anaphylaxis inhibition in a mouse-to-rat system in comparison with other methods.

Various methods have been employed for standardization of potency of allergen extracts. We used passive cutaneous anaphylaxis (PCA) inhibition in a mouse-to-rat system as a new means of standardization. Several allergen extracts, including mite, short ragweed, house dust, Aspergillus, Candida, and Japanese cedar, were examined. Mouse IgE antibodies were produced after two or three injections of antigen and alum. The potency measured by PCA inhibition in the mouse-to-rat system was compared with that of protein nitrogen (PN) content, end point of prick test in humans, and 50% radioallergosorbent test (RAST) inhibition. Our studies suggest that the mouse-to-rat system could be used to determine allergenic potency and to standardize allergen extracts.

Allergens↗
PubMed1977

Antigens in penicillin allergy. II. The influence of the number of penicilloyl residues on the antigenicity of macromolecules as determined by radioimmunoassay (RIA), passive cutaneous anaphylaxis (PCA) and antibody induction.

The present communication reveals a relationship between the epitope density of penicilloylated protein antigens and their antigenic activities in a radioimmunoassay (RIA), in passive cutaneous anaphylaxis (PCA) and in inducing antibody formation in mice. In the RIA and PCA a critical number of 2-4 penicilloyl residues per protein molecule was noted. At this level small changes in the number of substituents considerably influenced the antigenic activities. The molecular weight and the nature of the carrier proteins, myoglobin, bovine serum albumin (BSA) and dimeric BSA also affected the threshold concentration for efficient antigenic activity. The results with the RIA and PCA were significantly correlated to each other. Using penicilloylated BSA as immunizing antigen in mice it was found that an epitope number higher than 11 penicilloyl residues per protein molecule induced significant antibody formation after a single injection. Antigens with a lower degree of penicilloyl substitution were less immunogenic. An antigen carrying 0.6 penicilloyl residues per BSA molecule did not induce penicilloyl-specific antibodies even after three injections. The capacity of heavily penicilloylated proteins to induce and elicit penicillin allergy as revealed by the present results stresses the importance of limiting their presence in penicillin preparations.

Ampicillin↗
PubMed1975

Specificity and sensitivity of skin test reactions to extracts of Toxocara canis and Ascaris suum II. Homologous 48-hour passive cutaneous anaphylaxis tests with sera from infected guinea pigs.

The specificity and sensitivity of adult and larval somatic antigens and perienteric fluid of Toxocara canis and Ascaris suum were investigated by using a modified passive cutaneous anaphylaxis procedure in guinea pigs. Pooled sera from animals infected with low doses (0.01, 0.1, or 1.0 egg/g) were most reactive with the homologous larval antigen preparation. However, the Toxocara antisera were highly reactive with this antigen only, whereas the Ascaris antisera reactions could not be interpreted as being clearly positive with any of the antigen preparations. Sera from hyperinfected animals were also reactive with the homologous larval antigen. In addition, Ascaris larval antigen was reactive with Toxocara antiserum. The reciprocal relationship, i.e., reactivity of Toxocara larval antigen with Ascaris antiserum, was no apparent. In no instance did adult antigens induce reactions that could be interpreted as specific or sensitive indicators of antibody.

Animals↗
PubMed1979

On the latency period of sensitization: inhibition of passive cutaneous anaphylaxis by a factor in normal rat serum.

Addition of normal rat serum to mouse or rat IgE antibody blocks the passive cutaneous sensitization of rats with either IgE. The inhibition can be obtained with isologous and autologous rat serum. The blocking factor was purified and characterized as a molecule with a MW of 69,000 daltons, a sedimentation rate of 4.5 s and an isoelectric point of pH 4.7. The factor blocks the PCA reaction also at previously sensitized skin sites and seems to act on the secretory phase of mediator release.

Animals↗
PubMed1979

Inhibition of rat passive cutaneous anaphylaxis by 3-(tetrazol-5-yl)quinolines.

Quinoline-3-carboxylic acid (3) was found to have weak oral activity in the rat passive cutaneous (PCA) assay. In an effort to increase activity, the synthesis of structurally related compounds was initiated. This led to substituted 3-(tetrazol-5-yl)quinolines, some of which are equal in potency, when given orally, to doxantrazole. Further work resulted in the synthesis of 4-oxoquinolines, one of which, 8-chloro-1,4-dihydro-4-oxo-3-(tetrazol-5-yl)quinoline (132), is 33-fold more active than disodium cromoglycate (ip) and 32-fold more active than doxantrazole (po).

Animals↗