Antigen-induced release of slow reacting substance of anaphylaxis (SRS-A rat) in rats prepared with homologous antibody

The polymorphonuclear leukocyte appears to be an essential cellular prerequisite for the antigen-induced release of SRS-A(rat) in the peritoneal cavity of rats prepared with homologous, hyperimmune antisera. Depletion of PMN leukocytes is associated with a marked suppression of SRS-A(rat) release, w...

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Published inThe Journal of experimental medicine Vol. 127; no. 4; pp. 767 - 782
Main Authors Orange, R P, Valentine, M D, Austen, K F
Format Journal Article
LanguageEnglish
Published United States The Rockefeller University Press 01.04.1968
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Abstract The polymorphonuclear leukocyte appears to be an essential cellular prerequisite for the antigen-induced release of SRS-A(rat) in the peritoneal cavity of rats prepared with homologous, hyperimmune antisera. Depletion of PMN leukocytes is associated with a marked suppression of SRS-A(rat) release, whereas depletion of circulating lymphocytes or peritoneal mast cells does not influence the antigen-induced release of SRS-A(rat). A local increase in the number of PMN leukocytes produced by the induction of a peritoneal exudate was associated with an enhanced release of SRS-A(rat). A distinct difference in the cellular requirements for the antigen-induced release of histamine and SRS-A(rat) in the rat was observed. Homocytotropic antibody-mediated histamine release could be achieved in leukopenic rats but not in mast cell-depleted animals. Conversely, SRS-A(rat) release was suppressed in leukopenic rats but was unaffected by mast cell depletion. Diethylcarbamazine inhibited the antigen-induced release of SRS-A(rat) following preparation with homologous, hyperimmune antisera but did not interfere with homocytotropic antibody-mediated histamine release. In preventing SRS-A(rat) release, diethylcarbamazine did not interfere with antigen-antibody interaction since desensitization of tissues was possible in the presence of this inhibitor. This observation is consistent with the view that diethylcarbamazine inhibits the reaction sequence leading to the formation and release of SRS-A(rat) at some step subsequent to antigen-antibody interaction. These studies support the view that the immunologic pathways leading to the release of SRS-A(rat) and histamine in the rat are distinctly different in terms of the immunoglobulins involved, the cellular prerequisites, and the effective pharmacologic inhibitors.
AbstractList The polymorphonuclear leukocyte appears to be an essential cellular prerequisite for the antigen-induced release of SRS-A rat in the peritoneal cavity of rats prepared with homologous, hyperimmune antisera. Depletion of PMN leukocytes is associated with a marked suppression of SRS-A rat release, whereas depletion of circulating lymphocytes or peritoneal mast cells does not influence the antigen-induced release of SRS-A rat . A local increase in the number of PMN leukocytes produced by the induction of a peritoneal exudate was associated with an enhanced release of SRS-A rat . A distinct difference in the cellular requirements for the antigen-induced release of histamine and SRS-A rat in the rat was observed. Homocytotropic antibody-mediated histamine release could be achieved in leukopenic rats but not in mast cell-depleted animals. Conversely, SRS-A rat release was suppressed in leukopenic rats but was unaffected by mast cell depletion. Diethylcarbamazine inhibited the antigen-induced release of SRS-A rat following preparation with homologous, hyperimmune antisera but did not interfere with homocytotropic antibody-mediated histamine release. In preventing SRS-A rat release, diethylcarbamazine did not interfere with antigen-antibody interaction since desensitization of tissues was possible in the presence of this inhibitor. This observation is consistent with the view that diethylcarbamazine inhibits the reaction sequence leading to the formation and release of SRS-A rat at some step subsequent to antigen-antibody interaction. These studies support the view that the immunologic pathways leading to the release of SRS-A rat and histamine in the rat are distinctly different in terms of the immunoglobulins involved, the cellular prerequisites, and the effective pharmacologic inhibitors.
The polymorphonuclear leukocyte appears to be an essential cellular prerequisite for the antigen-induced release of SRS-A(rat) in the peritoneal cavity of rats prepared with homologous, hyperimmune antisera. Depletion of PMN leukocytes is associated with a marked suppression of SRS-A(rat) release, whereas depletion of circulating lymphocytes or peritoneal mast cells does not influence the antigen-induced release of SRS-A(rat). A local increase in the number of PMN leukocytes produced by the induction of a peritoneal exudate was associated with an enhanced release of SRS-A(rat). A distinct difference in the cellular requirements for the antigen-induced release of histamine and SRS-A(rat) in the rat was observed. Homocytotropic antibody-mediated histamine release could be achieved in leukopenic rats but not in mast cell-depleted animals. Conversely, SRS-A(rat) release was suppressed in leukopenic rats but was unaffected by mast cell depletion. Diethylcarbamazine inhibited the antigen-induced release of SRS-A(rat) following preparation with homologous, hyperimmune antisera but did not interfere with homocytotropic antibody-mediated histamine release. In preventing SRS-A(rat) release, diethylcarbamazine did not interfere with antigen-antibody interaction since desensitization of tissues was possible in the presence of this inhibitor. This observation is consistent with the view that diethylcarbamazine inhibits the reaction sequence leading to the formation and release of SRS-A(rat) at some step subsequent to antigen-antibody interaction. These studies support the view that the immunologic pathways leading to the release of SRS-A(rat) and histamine in the rat are distinctly different in terms of the immunoglobulins involved, the cellular prerequisites, and the effective pharmacologic inhibitors.
The polymorphonuclear leukocyte appears to be an essential cellular prerequisite for the antigen-induced release of SRS-Arat in the peritoneal cavity of rats prepared with homologous, hyperimmune antisera. Depletion of PMN leukocytes is associated with a marked suppression of SRS-Arat release, whereas depletion of circulating lymphocytes or peritoneal mast cells does not influence the antigen-induced release of SRS-Arat. A local increase in the number of PMN leukocytes produced by the induction of a peritoneal exudate was associated with an enhanced release of SRS-Arat. A distinct difference in the cellular requirements for the antigen-induced release of histamine and SRS-Arat in the rat was observed. Homocytotropic antibody-mediated histamine release could be achieved in leukopenic rats but not in mast cell-depleted animals. Conversely, SRS-Arat release was suppressed in leukopenic rats but was unaffected by mast cell depletion. Diethylcarbamazine inhibited the antigen-induced release of SRS-Arat following preparation with homologous, hyperimmune antisera but did not interfere with homocytotropic antibody-mediated histamine release. In preventing SRS-Arat release, diethylcarbamazine did not interfere with antigen-antibody interaction since desensitization of tissues was possible in the presence of this inhibitor. This observation is consistent with the view that diethylcarbamazine inhibits the reaction sequence leading to the formation and release of SRS-Arat at some step subsequent to antigen-antibody interaction. These studies support the view that the immunologic pathways leading to the release of SRS-Arat and histamine in the rat are distinctly different in terms of the immunoglobulins involved, the cellular prerequisites, and the effective pharmacologic inhibitors.
Author Austen, K F
Valentine, M D
Orange, R P
AuthorAffiliation From the Department of Medicine, Harvard Medical School at the Robert B. Brigham Hospital, Boston, Massachusetts 02120
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Snippet The polymorphonuclear leukocyte appears to be an essential cellular prerequisite for the antigen-induced release of SRS-A(rat) in the peritoneal cavity of rats...
The polymorphonuclear leukocyte appears to be an essential cellular prerequisite for the antigen-induced release of SRS-Arat in the peritoneal cavity of rats...
The polymorphonuclear leukocyte appears to be an essential cellular prerequisite for the antigen-induced release of SRS-A rat in the peritoneal cavity of rats...
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pubmed
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StartPage 767
SubjectTerms Animals
Antibodies - analysis
Antigens
Autacoids - metabolism
Complement System Proteins - analysis
Diethylcarbamazine - pharmacology
Histamine - metabolism
Immune Sera
Injections, Intraperitoneal
Leukocytes - immunology
Leukocytes - physiology
Lymphocytes - immunology
Male
Mast Cells - physiology
Mechlorethamine - pharmacology
Muscle, Smooth - physiology
Ovalbumin
Passive Cutaneous Anaphylaxis
Rabbits
Rats
Serum Albumin, Bovine
Species Specificity
Venoms
Title Antigen-induced release of slow reacting substance of anaphylaxis (SRS-A rat) in rats prepared with homologous antibody
URI https://www.ncbi.nlm.nih.gov/pubmed/4384530
https://pubmed.ncbi.nlm.nih.gov/PMC2138477
Volume 127
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