Disease relevance of Pcas

• Strikingly, these mice lack IgG-mediated mast cell degranulation, are resistant to IgG-dependent passive cutaneous anaphylaxis, and exhibit an impaired Arthus reaction [1].
• Heat-inactivated immune serum induced passive cutaneous anaphylaxis, suggesting that anaphylaxis in C3H mice was mediated by IgG1 [2].
• We report that LPS administration suppresses the IgE-mediated and mast cell-dependent passive cutaneous anaphylaxis, pulmonary inflammation, airway eosinophilia, mucus production, and airway hyperactivity [3].
• To investigate the effects of these substances in vivo, models of passive cutaneous anaphylaxis and atopic dermatitis mice (NC/Nga) were used [4].
• New 1-(2-pyridinyl)piperazine derivatives were synthesized and tested as inhibitors of the reaginic passive cutaneous anaphylaxis in the rat (PCA), of the histamine-induced bronchospasm in the guinea pig, and of the rat mesenteric mast cell degranulation induced by compound 48/80 [5].

Psychiatry related information on Pcas

• On the latency period of sensitization: inhibition of passive cutaneous anaphylaxis by a factor in normal rat serum [6].

High impact information on Pcas

• Thus these mice failed to mount IgE antibody responses to either keyhole limpet hemocyanin or ovalbumin challenge, assessed by the passive cutaneous anaphylaxis reaction [7].
• 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 [8].
• The titers, measured by passive cutaneous anaphylaxis in rats, increased after repeated applications of picryl chloride [9].
• Targeted disruption of the histidine decarboxylase gene (HDC(-/-)), the only histamine-synthesizing enzyme, led to a histamine-deficient mice characterized by undetectable tissue histamine levels, impaired gastric acid secretion, impaired passive cutaneous anaphylaxis, and decreased mast cell degranulation [10].
• The Mc-cpa-/- mast cell phenotype was not associated with defects in degranulation in vitro or passive cutaneous anaphylaxis in vivo [11].

Chemical compound and disease context of Pcas

• When the mAb was applied during a topical booster sensitization, the nasal eosinophilia, the 8-day PCA titer and histamine hypersensitivity were significantly suppressed in the treated animals [12].
• Quinotolast potently inhibited such type I allergic reactions as passive cutaneous anaphylaxis (PCA) and anaphylactic bronchoconstriction in rats by both intravenous and oral dosing [13].
• Homologous passive cutaneous anaphylaxis (PCA) and active cutaneous anaphylaxis (ACA) to ovalbumin and DNP-hapten were studied in the ears of female BALB/c mice by means of assessing Evans blue dye leakage [14].
• Ear thickness, contact hypersensitivity (CH) induced by topical application of picryl chloride (PC) or oxazolone (Ox) after sensitization, and vascular permeability after ear passive cutaneous anaphylaxis (PCA) were compared between wild-type (WT) and PAR-2(-/-) mice [15].
• AA-344 showed inhibitory effects on the homologous passive cutaneous anaphylaxis and the passive systemic anaphylaxis in guinea pigs [16].

Biological context of Pcas

• The strain difference and mode of inheritance of the susceptibility to PCA (passive cutaneous anaphylaxis) were studied in mice [17].
• The increased vascular permeability associated with IgE-dependent passive cutaneous anaphylaxis was significantly reduced in CysLT(2) receptor-null mice as compared with wild-type mice, whereas plasma protein extravasation in response to zymosan A-induced peritoneal inflammation was not altered [18].
• Reduced IgE antibody titer, measured by passive cutaneous anaphylaxis, decreased hemagglutination titer to sheep red blood cells, blocked histamine release from mixed peritoneal cells of rats in vitro induced by antigen, but had no significant effect when histamine release was induced by compound 48/80 [19].
• Several peptide fragments located in the amino acid sequences Ala329-Thr357 and Arg419-Ala463, inhibited passive cutaneous anaphylaxis (PCA) in vivo [20].
• Both IL-3 -/- and +/+ mice expressed equivalent IgE-dependent passive cutaneous anaphylaxis responses following challenge with specific antigen and exhibited equivalent active systemic anaphylaxis responses to ovalbumin as assessed by changes in body temperature, death rates, total IgE production, and histamine release [21].

Anatomical context of Pcas

• The microtubule depolymerizers attenuated the passive cutaneous anaphylaxis reaction in back skin of Sprague Dawley rats [22].
• Anti-SEA responses include lymphocyte blastogenesis, the production of the lymphokine eosinophil stimulation promoter (ESP), hemagglutinating antibody, heat-labile and heat-stable, 72-hr passive cutaneous anaphylaxis (PCA) antibodies, and pronounced peripheral blood eosinophilia [23].
• Sera were analyzed for IgG subclasses by ELISA for anaphylactic IgE by rat basophil degranulation, and after heat inactivation of IgE for anaphylactic IgG by passive cutaneous anaphylaxis assay [24].
• The two kinds of antibodies appeared to be specific for different antigens because the agglutinin, but not IgE, could be removed by absorbing the serum with a polysaccharide from the cell wall of C. albicans, but the polysaccharide did not provoke the PCA reaction [25].
• A remarkable difference between PCA in W/Wv and reference mice was also observed in the susceptibility to monoclonal anti-mouse granulocyte (Gr-1) antibody: PCA in W/Wv mice was potently suppressed by the 1- to 3-day pretreatment with this antibody but that in references was not at all [26].

Associations of Pcas with chemical compounds

• The fractions were assayed in vivo by passive cutaneous anaphylaxis in rats, and for histamine or serotonin release in vitro using normal or tumor mouse mast cells [27].
• The PMA-induced dermal mast cells in W/Wv mice appeared mature by morphology, stained with the heparin-binding fluorescent dye, berberine sulfate, and were competent to express IgE-dependent passive cutaneous anaphylaxis responses [28].
• The Mr 14,000 molecule was also found to be a potent allergen in a passive cutaneous anaphylaxis assay, and the IgE response to it was also restricted to H-2s [29].
• Interestingly, orally administered histamine was distributed in the skin in HDC-/- mice and in these histamine-supplemented mice the plasma extravasation reaction was observed after the injection of compound 48/80 and the PCA test [30].
• PCA in W/Wv mice mediated by a low dilution (1:4) of hyperimmune serum to bovine serum albumin of the B6D2F1 mouse origin was markedly suppressed by CV-6209, an antagonist of platelet-activating factor (PAF), but not by antihistamines such as cyproheptadine and oxatomide [26].

Regulatory relationships of Pcas

• Synthetic antisense Fc epsilon RI alpha ODN dose-dependently inhibited passive cutaneous anaphylaxis and histamine release from the mouse peritoneal mast cells (MPMC) activated by anti-dinitrophenyl (DNP) IgE [31].

Other interactions of Pcas

• IgG1 and IgE antibodies produced during primary and secondary responses were measured by passive cutaneous anaphylaxis [32].
• BW also inhibited vascular permeability increase caused by passive cutaneous anaphylaxis and histamine, and ear swelling caused by tumor necrosis factor-alpha [33].
• In addition, Bcl10-deficient mice display impaired IgE-mediated passive cutaneous anaphylaxis [34].
• Attenuated zymosan-induced peritoneal vascular permeability and IgE-dependent passive cutaneous anaphylaxis in mice lacking leukotriene C4 synthase [35].
• By contrast, IL-9 did not increase the susceptibility to passive cutaneous anaphylaxis [36].

Analytical, diagnostic and therapeutic context of Pcas

• Significant PCA reactions were elicited, however, with PI-specific IgG1 from IL-12-/- or anti-IFN-gamma Ab-treated mice, although less Ab was measured by ELISA [37].
• Depletion with anti-IL-4 antibody led to profound suppression of IgE-eosinophil-mediated antibody-dependent cell-mediated cytotoxicity and passive cutaneous anaphylaxis responses against the parasite and no effect on IgG2a antibody, Ag-mediated blast transformation, or resistance [38].
• The recombinant protein is able to induce a passive cutaneous anaphylaxis reaction in rat, and it behaves similarly to the native Equ c1 in several immunological tests with allergic patients' IgE antibodies, mouse monoclonal antibodies, or rabbit polyclonal IgG antibodies [39].
• 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 [40].
• 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 [41].

References