scholarly journals ANTIGEN-INDUCED RELEASE OF SLOW REACTING SUBSTANCE OF ANAPHYLAXIS (SRS-ARAT) IN RATS PREPARED WITH HOMOLOGOUS ANTIBODY

1968 ◽  
Vol 127 (4) ◽  
pp. 767-782 ◽  
Author(s):  
Robert P. Orange ◽  
Martin D. Valentine ◽  
K. Frank Austen
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Reaction Sequence ◽  
Peritoneal Mast Cells ◽  
Pmn Leukocytes ◽  
Circulating Lymphocytes ◽  
Pharmacologic Inhibitors ◽  
Antigen Antibody ◽  
Marked Suppression

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.

scholarly journals MECHANISMS OF IMMUNOLOGIC INJURY OF RAT PERITONEAL MAST CELLS

1966 ◽  
Vol 124 (3) ◽  
pp. 379-395 ◽  
Author(s):  
Elmer L. Becker ◽  
K. Frank Austen
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Guinea Pig ◽  
Histamine Release ◽  
Response Curve ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells ◽  
Logarithmic Relationship ◽  
Antigen Antibody ◽  
The Complement System

The ability of a number of p-nitrophenylethyl, alkyl phenylalkyl, chloroalkyl, and aminoalkyl phosphonates to inhibit the homocytotropic antibody-mediated release of histamine from rat peritoneal mast cells has been tested. The effectiveness of these same phosphonates against the activated first component of rat complement (C'1a) has also been investigated. The rat mast cell esterase activated by the reaction of antigen and homocytotropic antibody resembles chymotrypsin in its reactivity with the phenylalkyl and chloroalkyl phosphonate, but is unlike this protease in its greater responsiveness to the 5-aminopentyl phosphonate relative to the pentyl phosphonate. The antigen-homocytotropic antibody-activated mast cell esterase and chymotrypsin, thus, appear to be similar, but different enzymes; i.e., they are parazymes (see reference 4, p. 501). There are distinct differences in the pattern of inhibition given by the phenylalkyl and aminoalkyl and alkyl phosphonates of the homocytotropic antibody-mediated histamine release from rat peritoneal mast cells and from guinea pig lung slices. On the basis of these differences it is concluded that the esterases activated by the combination of antigen and homocytotropic antibody on the mast cells of the two species are not the same. The arithmetic dose response curve found for the action of the phosphonates on the antigen-induced histamine release from rat peritoneal mast cells contrasted sharply with the logarithmic relationship found when these same inhibitors acted on the guinea pig lung system. This suggests that in addition to the antigen-antibody-activated esterases being unlike, the detailed mode of histamine release from the mast cells of the guinea pig lung differs from that of the mast cells of the rat peritoneum. Distinct and large differences were found in the pattern of inhibition of histamine release from rat peritoneal mast cells and of rat C'1a given by the phenylalkyl, and chloroalkyl and alkyl phosphonates implying that esterase activated by the combination of antigen with the sensitized rat peritoneal mast cells is not C'1a. Thus, the results with the peritoneal mast cells lead to the same conclusion as the previous work with guinea pig lung slices; i.e., the antigen-antibody-activated esterase involved in the homocytotropic antibody-mediated release of histamine is not part of the complement system.

scholarly journals Anti-immunoglobulin-induced histamine secretion by rat peritoneal mast cells studied by immunoferritin electron microscopy.

1975 ◽  
Vol 142 (2) ◽  
pp. 391-402 ◽  
Author(s):  
D Lawson ◽  
C Fewtrell ◽  
B Gomperts ◽  
M Raff
Keyword(s):  
Electron Microscopy ◽  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Histamine Secretion ◽  
Calcium Dependent ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells

We have used ferritin-conjugated divalent and monovalent anti-Ig antibodies to study simultaneously, histamine secretion and the ultrastructural distribution and redistribution of Ig receptors on rat peritoneal mast cells. We conclude that (a) divalent anti-Ig is required for both receptor redistribution and for calcium-dependent degranulation and histamine release, (b) divalent anti-Ig induces patching and pinocytosis but not capping of Ig molecules, (c) neither capping nor pinocytosis are required for triggering and if clustering is necessary, then less than 10 Ig molecules are required per cluster, and (d) degranulation (and histamine release) is not an all or none response of the mast cell.

Modulatory action of potassium channel openers on field potential and histamine release from rat peritoneal mast cells

2009 ◽  
Vol 87 (8) ◽  
pp. 624-632 ◽  
Author(s):  
Chi-Kong Yeung ◽  
Jessica Ka-Yan Law ◽  
Sze-Wing Sam ◽  
Sven Ingebrandt ◽  
Hang-Yung Alaster Lau ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Potassium Channel ◽  
Histamine Release ◽  
Field Potential ◽  
Peritoneal Mast Cell ◽  
Induced Response ◽  
Potassium Channel Openers ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells

To determine whether changes in membrane potential affect the extent of mast cell degranulation, compound 48/80 was added to rat peritoneal mast cell suspensions in the absence or presence of potassium channel openers (KCOs). Changes were compared between the field potential (FP) and the amount of histamine released. The results demonstrated that (i) the onset and duration of FP, which reflects the hyperpolarizing nature of the response, increased as the concentration of compound 48/80 increased; (ii) both FP and the amount of histamine released increased as the concentration of compound 48/80 increased; (iii) although both KCOs (SDZ PCO400, a benzopyran derivative, and P1060, a cyanoguanidine derivative) potentiated compound 48/80-induced increases in FP and histamine release, without compound 48/80, they had no effect on either parameter; (iv) both glibenclamide and charybdotoxin significantly attenuated the compound 48/80-induced increase in FP; and (v) glibenclamide was able to attenuate the KCO-induced potentiation of FP. The results show that drugs presumably causing hyperpolarization can affect histamine release from rat peritoneal mast cells. The effect of KCOs on compound 48/80-induced response appears to be potentiation in nature rather than synergism. It is possible that KCO hyperpolarizes the cell membrane, enhances Ca2+ influx, and thus increases histamine release. As such, selective blockers of K+ channels may be useful for the treatment of immunological disorders.

scholarly journals MECHANISMS OF IMMUNOLOGIC INJURY OF RAT PERITONEAL MAST CELLS

1966 ◽  
Vol 124 (3) ◽  
pp. 397-416 ◽  
Author(s):  
K. Frank Austen ◽  
Elmer L. Becker
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Gamma Globulin ◽  
Experimental Conditions ◽  
Complement Components ◽  
Precursor State ◽  
Absolute Requirement ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells ◽  
Antigen Antibody

There is an absolute requirement for C'1, C'2, C'4, C'3, and C'5 in releasing histamine from rat peritoneal mast cells sensitized with rabbit anti-rat gamma globulin. This conclusion is based upon the restoration of histamine-releasing capacity by adding highly purified complement components to sera deficient in one or more of these components. Of special advantage was the availability of sera from humans with inborn or acquired deficiencies in a single component. The p-nitrophenyl ethyl phosphonates block this reaction by inhibiting an antigen-antibody-activated esterase which exists in a phosphonate resistant precursor state until activated by the interaction of the sensitized mast cell and serum complement. There is almost complete disparity between the ability of the phosphonates to inhibit complement-dependent histamine release by rabbit anti-RGG and to inactivate C'1a. Even though C'1a is required for complement-dependent histamine release by rabbit anti-RGG, this is not the esterase being blocked by the phosphonates under the experimental conditions used. The pattern of inhibition by the phosphonates of the antigen-antibody-activated esterase required for complement-dependent, noncytotoxic histamine release is remarkably similar to that of the esterase required for homocytotropic antibody-mediated histamine release. One possible implication is that these two quite different modes of carrying out antigen-antibody-induced histamine release from rat peritoneal mast cells lead to activation of the same esterase and share a common pathway.

Inhibitions of mast cell-derived histamine release by different Flos Magnoliae species in rat peritoneal mast cells

Phytomedicine ◽  
2008 ◽  
Vol 15 (10) ◽  
pp. 808-814 ◽  
Author(s):  
Y. Shen ◽  
E.C.K. Pang ◽  
C.C.L. Xue ◽  
Z.Z. Zhao ◽  
J.G. Lin ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells
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