Glycogenolysis and control of anaphylactic histamine release by cyclic adenosine monophosphate-related agents *1, *2II. Modification of histamine release by glycogenolytic metabolites

Okazaki, Tadao; Okazaki, Atsuyuki; Reisman, Robert E.; Arbesman, Carl E.

doi:10.1016/0091-6749(75)90099-8

Cited by 4 publications

(5 citation statements)

References 9 publications

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“…For example, the concentrations of pyruvate ( Pleshkova and Tsvetkova, 1978 ) and ATP ( Norn et al ., 1976 ) are lower in mast cells after antigen challenge. Histamine release is inhibited by the non‐metabolizable glucose analogue, 2‐deoxyglucose ( Chakravarty, 1967 ) and by glycogenolytic intermediates ( Okazaki et al ., 1975 ). Moreover, lower pyruvate kinase (PK) activity has been reported in patients with atopic dermatitis ( Miklaszewska et al ., 1989 ) and eczema ( Buchtova and Cech, 1982 ).…”

Section: Introductionmentioning

confidence: 99%

Regulation of M₂‐type pyruvate kinase mediated by the high‐affinity IgE receptors is required for mast cell degranulation

Ryu

Walker

Kim

et al. 2008

British J Pharmacology

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Background and purpose: M 2 -type pyruvate kinase (M 2 PK) was found to interact directly with the 'ITAM' region of the g chain of the high-affinity IgE receptor (FceRI). Our hypothesis was that mast cell degranulation might require the FceRImediated inhibition of M 2 PK activity. Experimental approach: In rat basophilic leukaemia (RBL-2H3) cells, the effects of directly inhibiting M 2 PK or preventing the FceRI-mediated inhibition of M 2 PK (disinhibition) on degranulation was measured by hexosaminidase release. Effects of blocking the FceRI-mediated inhibition of M 2 PK was also assessed in vivo in a mouse model of allergen-induced airway hyperresponsiveness. Key results: Activation of FceRI in RBL-2H3 cells caused the rapid phosphorylation of tyrosine residues in M 2 PK, associated with a decrease in M 2 PK enzymatic activity. There was an inverse correlation between M 2 PK activity and mast cell degranulation. FceRI-mediated inhibition of M 2 PK involved Src kinase, phosphatidylinositol 3-kinase, PKC and calcium. Direct inhibition of M 2 PK potentiated FceRI-mediated degranulation and prevention of the FceRI-mediated inhibition of M 2 PK attenuated mast cell degranulation. Transfection of RBL-2H3 cells with M 1 PK which prevents FceRI-induced inhibition of M 2 PK, markedly reduced their degranulation and exogenous M 1 PK (i.p.) inhibited ovalbumin-induced airway hyper-responsiveness in vivo. Conclusions and implications:We have identified a new control point and a novel biochemical pathway in the process of mast cell degranulation. Our study suggests that the FceRI-mediated inhibition of M 2 PK is a crucial step in responses to allergens. Moreover, the manipulation of glycolytic processes and intermediates could provide novel strategies for the treatment of allergic diseases.

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Section: Introductionmentioning

confidence: 99%

Regulation of M₂‐type pyruvate kinase mediated by the high‐affinity IgE receptors is required for mast cell degranulation

Ryu

Walker

Kim

et al. 2008

British J Pharmacology

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“…In each experiment, lung fragments from 3 or 4 animals were pooled, and 2-4 samples were pre pared for each particular experimental condition. The in vitro sensitization and subsequent chal lenge of monkey lung fragments [9] was per formed essentially in the same way as that de scribed above for guinea pig lung fragments. …”

Section: Passive Sensitization and Antigenic Histaminementioning

confidence: 62%

“…was the immunizing antigen for the preparation of anti-CEA antisera by the same method as used for BSA. Undialyzed pooled human reaginic serum with Prausnitz-Kiistner titers higher than 1:1,000 against crude ragweed pollen antigen were used for the passive sensitization of fragments of rhesus monkey lung as previously described [9], Purification of Anti-BSA Antibody Purification of anti-BSA antibody was per formed using BSA-Sepharose immunoadsorbent [10]. BSA was coupled to Sepharose 4B (cyanogen bromide activated, Pharmacia Fine Chemicals, AB, Uppsala, Sweden) by adding the latter to the BSA solution in 0.1 M NaHC03 and gently stir ring the mixture at 4 °C for 16 h. The immunoad sorbent was then washed with 0.5 M acetic acid, and suspended in the pooled anti-BSA serum for 15 min.…”

Section: Preparation Of Antiseramentioning

confidence: 99%

Optimal Antibody-Receptor Ratio in Anaphylactic-Sensitization

Okazaki¹,

Fujita²,

Okazaki³

et al. 1977

Int Arch Allergy Immunol

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The antigen-induced release of histamine from guinea pig and monkey lung fragments sensitized in vitro with hyperimmune rabbit antibody and human reaginic serum, respectively, was studied. When the amounts of whole antiserum, γ-globulin fraction, or purified antibody were increased over the optimum in passive anaphylactic sensitization, the subsequent histamine release was reduced in spite of the fact that proportionately greater amounts of antigen were added to the system. The observed inhibition by higher antibody concentrations might be due to a reduction in cell-stimulating capacity of the antigen-antibody-receptor complex caused by inappropriate ratios among any of these three components.

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“…Since previous investigators [8,18] have used different buffers (phosphate or bicar bonate), it was not clear whether air or (95% + 5% C 0 2) is superior for generating AIR from guinea pig lung slices. Therefore, the effect of the composition of gas phase on AIR was examined.…”

Section: Effect Of Composition Of Gas Phase On Antigen-induced Histammentioning

confidence: 99%

“…It has been pre viously reported [6,18] that histamine re lease starts within seconds after the addition of the antigen and that the release is com plete within 5-10 min. In one experiment it was confirmed that 40-60% of the AIR oc curred in the first 2 min and that the pro cess was complete within 15 min.…”

Section: Effect Of Time On Antigen-induced Histamine Releasementioning

confidence: 99%

Antigen-Induced Release of Histamine from Passively Sensitized Guinea Pig Lung Slices

Khandwala¹,

Damiani²,

Weinryb³

1979

Int Arch Allergy Immunol

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The effect of several parameters (pH, Ca⁺⁺ concentration, time, temperature, lung slice size) on in vitro antigen-induced histamine release from passively sensitized guinea pig lung slices was investigated. With respect to pH, Ca⁺⁺ concentration and time, the optimal conditions for the passive sensitization step (pH 7.8, Ca⁺⁺ 1.5 mM, 2 h) were distinctly different from those for the antigen challenge step (pH 8.2, Ca⁺⁺ 10 mM, 15 min). Maximum antigen-induced release was obtained with 3 × 0.25 × 0.25 mm lung slices at 37 °C using air as gas phase.

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Glycogenolysis and control of anaphylactic histamine release by cyclic adenosine monophosphate-related agents 1, 2II. Modification of histamine release by glycogenolytic metabolites

Cited by 4 publications

References 9 publications

Regulation of M₂‐type pyruvate kinase mediated by the high‐affinity IgE receptors is required for mast cell degranulation

Regulation of M₂‐type pyruvate kinase mediated by the high‐affinity IgE receptors is required for mast cell degranulation

Optimal Antibody-Receptor Ratio in Anaphylactic-Sensitization

Antigen-Induced Release of Histamine from Passively Sensitized Guinea Pig Lung Slices

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Glycogenolysis and control of anaphylactic histamine release by cyclic adenosine monophosphate-related agents *1, *2II. Modification of histamine release by glycogenolytic metabolites

Cited by 4 publications

References 9 publications

Regulation of M2‐type pyruvate kinase mediated by the high‐affinity IgE receptors is required for mast cell degranulation

Regulation of M2‐type pyruvate kinase mediated by the high‐affinity IgE receptors is required for mast cell degranulation

Optimal Antibody-Receptor Ratio in Anaphylactic-Sensitization

Antigen-Induced Release of Histamine from Passively Sensitized Guinea Pig Lung Slices

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Product

Resources

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Glycogenolysis and control of anaphylactic histamine release by cyclic adenosine monophosphate-related agents 1, 2II. Modification of histamine release by glycogenolytic metabolites

Regulation of M₂‐type pyruvate kinase mediated by the high‐affinity IgE receptors is required for mast cell degranulation

Regulation of M₂‐type pyruvate kinase mediated by the high‐affinity IgE receptors is required for mast cell degranulation