Effects of ADP-ribosylation of GTP-binding protein by pertussis toxin on immunoglobulin E-dependent and -independent histamine release from mast cells and basophils

H. Saito, F. Okajima, T. F P Molski, R. I. Sha'afi, M. Ui, T. Ishizaka

Research output: Contribution to journalArticle

Abstract

Pretreatment of rat peritoneal mast cells, human basophils, bone marrow-derived mouse mast cells (BMMC) and mouse mast cell line PT-18 cells with 1 μg/ml pertussis toxin (PT) failed to inhibit immunoglobulin E (IgE)-dependent histamine release from the cells. In BMMC and PT-18 cells, even 20-hr incubation of the cells with 1 μg/ml PT, which ADP-ribosylates more than 97% of 41 kDa, α-subunit of Ni in the cells, failed to affect the IgE-dependent release of histamine or arachidonate. The results indicate that GTP-binding protein, Ni, is not involved in the transduction of triggering signals induced by cross-linking of IgE receptors. In contrast, pretreatment of rat mast cells with 1 ng/ml to 0.1 μg/ml PT for 2 hr inhibited histamine release induced by compound 48/80 in a dose-dependent manner. A similar pretreatment with PT inhibited thrombin-induced histamine release from BMMC and N-formyl-L-methionyl-L-leucyl-L-phenylalanine-induced histamine release from human basophils in a similar dose-dependent fashion. However, even 20 hr of incubation of sensitized BMMC with 1 μg/ml PT failed to inhibit either thrombin-induced or antigen-induced breakdown of phosphatidylinositides (PI), i.e., the formation of inositol triphosphate and diacylglycerol, Quin-2 signal, and the release of arachidonic acid. The results indicate that the inhibition of thrombin-induced histamine release by PT-treatment is not due to the inhibition of PI-turnover, and that Ni is not involved in thrombin-induced or antigen-induced (IgE-dependent) hydrolysis of phosphatidylinositides in mast cells.

Original languageEnglish (US)
Pages (from-to)3927-3934
Number of pages8
JournalJournal of Immunology
Volume138
Issue number11
StatePublished - 1987
Externally publishedYes

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Basophils
Histamine Release
Pertussis Toxin
GTP-Binding Proteins
Mast Cells
Adenosine Diphosphate
Immunoglobulin E
Thrombin
Bone Marrow
leucyl-phenylalanine
p-Methoxy-N-methylphenethylamine
IgE Receptors
Antigens
Diglycerides
Inositol
Phenylalanine
Arachidonic Acid
Signal Transduction
Hydrolysis
Cell Line

ASJC Scopus subject areas

  • Immunology

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Effects of ADP-ribosylation of GTP-binding protein by pertussis toxin on immunoglobulin E-dependent and -independent histamine release from mast cells and basophils. / Saito, H.; Okajima, F.; Molski, T. F P; Sha'afi, R. I.; Ui, M.; Ishizaka, T.

In: Journal of Immunology, Vol. 138, No. 11, 1987, p. 3927-3934.

Research output: Contribution to journalArticle

Saito, H. ; Okajima, F. ; Molski, T. F P ; Sha'afi, R. I. ; Ui, M. ; Ishizaka, T. / Effects of ADP-ribosylation of GTP-binding protein by pertussis toxin on immunoglobulin E-dependent and -independent histamine release from mast cells and basophils. In: Journal of Immunology. 1987 ; Vol. 138, No. 11. pp. 3927-3934.
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abstract = "Pretreatment of rat peritoneal mast cells, human basophils, bone marrow-derived mouse mast cells (BMMC) and mouse mast cell line PT-18 cells with 1 μg/ml pertussis toxin (PT) failed to inhibit immunoglobulin E (IgE)-dependent histamine release from the cells. In BMMC and PT-18 cells, even 20-hr incubation of the cells with 1 μg/ml PT, which ADP-ribosylates more than 97{\%} of 41 kDa, α-subunit of Ni in the cells, failed to affect the IgE-dependent release of histamine or arachidonate. The results indicate that GTP-binding protein, Ni, is not involved in the transduction of triggering signals induced by cross-linking of IgE receptors. In contrast, pretreatment of rat mast cells with 1 ng/ml to 0.1 μg/ml PT for 2 hr inhibited histamine release induced by compound 48/80 in a dose-dependent manner. A similar pretreatment with PT inhibited thrombin-induced histamine release from BMMC and N-formyl-L-methionyl-L-leucyl-L-phenylalanine-induced histamine release from human basophils in a similar dose-dependent fashion. However, even 20 hr of incubation of sensitized BMMC with 1 μg/ml PT failed to inhibit either thrombin-induced or antigen-induced breakdown of phosphatidylinositides (PI), i.e., the formation of inositol triphosphate and diacylglycerol, Quin-2 signal, and the release of arachidonic acid. The results indicate that the inhibition of thrombin-induced histamine release by PT-treatment is not due to the inhibition of PI-turnover, and that Ni is not involved in thrombin-induced or antigen-induced (IgE-dependent) hydrolysis of phosphatidylinositides in mast cells.",
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AU - Saito, H.

AU - Okajima, F.

AU - Molski, T. F P

AU - Sha'afi, R. I.

AU - Ui, M.

AU - Ishizaka, T.

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