Biochemical analysis of glucocorticoid-induced inhibition of IgE-mediated histamine release from mouse mast cells.
J Immunol
; 129(3): 1212-8, 1982 Sep.
Article
em En
| MEDLINE
| ID: mdl-6180000
ABSTRACT
Pretreatment of mouse mast cells with 10(-7) to 10(-6) M dexamethasone (DM) during overnight sensitization with mouse IgE antibody resulted in inhibition of antigen-induced histamine release and degranulation. The inhibition of both degranulation and histamine release increased linearly with the duration of the treatment; maximal inhibition was obtained after approximately 16 hr with DM. The addition of DM to sensitized mast cells immediately before antigen challenge did not affect the antigen-induced histamine release. DM interacted directly with mast cells by binding to DM-specific cytoplasmic receptors. The treatment of mast cells with DM did not affect the binding of IgE to mast cells or intracellular cAMP levels. Bridging of cell-bound IgE anti-DNP antibody on mouse mast cells either by multivalent DNP-HSA or by anti-IgE induced phospholipid methylation at the plasma membrane and Ca++ influx into the cells. Pretreatment of mast cells with DM inhibited the antigen-induced phospholipid methylation and Ca++ uptake but failed to affect histamine release by Ca++ ionophore A23187. The results suggest that DM treatment inhibits histamine release by the inhibition of the early stage of biochemical processes leading to opening Ca++ channels but does not affect the process distal to Ca++ influx or the binding of IgE molecules to IgE receptors.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Imunoglobulina E
/
Glucocorticoides
/
Liberação de Histamina
/
Mastócitos
Limite:
Animals
Idioma:
En
Revista:
J Immunol
Ano de publicação:
1982
Tipo de documento:
Article