Decrease in IgE Fc receptor expression on mouse bone marrow-derived mast cells and inhibition of PAF-acether formation and of β-hexosaminidase release by dexamethasone

M. Benhamou, E. Ninio, P. Salem, C. Hieblot, G. Bessou, C. Pitton, Fu-Tong Liu, J. M. Mencia-Huerta

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

The effect of dexamethasone (DM) on the immunologic and nonimmunologic release of paf-acether and of the granule marker β-hexosaminidase (BHEX) from mouse bone marrow-derived mast cells (BMMC) was studied. BMMC (1 x 106) in a modified Tyrode's solution containing 0.25% bovine serum albumin (BSA) were sensitized with an optimal dose of dinitrophenyl (DNP)-specific monoclonal IgE, and were washed before challenge with 40 ng/ml of DNP coupled to BSA. Preincubation of BMMC for 24 hr with 1 nM to 1 μM DM inhibited in a dose-dependent fashion the immunologic release of paf-acether and of BHEX as compared with control cells, with a half-maximal effect at 20 nM and 4 nM respectively. By contrast, the ionophore A23187 (1 μM)-induced release of paf-acether and of BHEX was unaffected by DM pretreatment. Finally, the antigen-induced increase in acetyltransferase activity, used as an index of cellular activation, was inhibited by 37 ± 16% in 1 μM DM-treated BMMC as compared with untreated cells. Preincubation of BMMC with DM for 24 hr caused a dose-dependent inhibition of 125I-IgE binding to the cells, with a half-maximal effect at 14 nM. As determined by Scatchard analysis, the number of IgE Fc receptors was decreased by 55% in 1 μM DM-treated BMMC as compared with untreated cells, although the dissociation constants were comparable (control: 12.6 ± 4.1 nM; DM-treated cells: 14.1 ± 6.7 nM; mean ± SD; n = 3). Cytofluorometer analysis of BMMC sensitized with a saturating amount of purified monoclonal IgE, followed by addition of a fluoresceinated anti-mouse IgG (heavy and light chains), revealed a single cellular population for both DM-treated and untrated BMMC. This demonstrates that the DM-induced decrease in IgE Fc receptor expression was exhibited by every BMMC. The possible link between the decreased sensitization of the cells consequent to the reduction in IgE Fc receptor expression and the alteration of the secretory response and acetyltransferase activity was investigated. BMMC were incubated with IgE under experimental conditions giving half-sensitization of the cells. Upon antigen challenge, a 10.5 ± 3.7% decrease in acetyltransferase activity and a 29.2 ± 3.5% decrease in paf-acether release were observed with half-sensitized cells as compared with cells sensitized with a saturating amount of IgE. This result indicates that the decreased sensitization of the cells do not fully account for the inhibitions of paf-acether release and acetyltransferase activity observed upon DM treatment. These results indicate that DM inhibits the immunologic release of paf-acether and of BHEX from passively sensitized BMMC and decreases the IgE Fc receptor number available for sensitization. Thus, the modulation of IgE Fc receptor number could explain part of the anti-allergic properties of glucocorticosteroids.

Original languageEnglish (US)
Pages (from-to)1385-1392
Number of pages8
JournalJournal of Immunology
Volume136
Issue number4
StatePublished - 1986
Externally publishedYes

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IgE Receptors
Hexosaminidases
Fc Receptors
Platelet Activating Factor
Mast Cells
Dexamethasone
Bone Marrow
Acetyltransferases
Immunoglobulin E
Bovine Serum Albumin
Antigens
Anti-Allergic Agents
Ionophores
Calcimycin

ASJC Scopus subject areas

  • Immunology

Cite this

Benhamou, M., Ninio, E., Salem, P., Hieblot, C., Bessou, G., Pitton, C., ... Mencia-Huerta, J. M. (1986). Decrease in IgE Fc receptor expression on mouse bone marrow-derived mast cells and inhibition of PAF-acether formation and of β-hexosaminidase release by dexamethasone. Journal of Immunology, 136(4), 1385-1392.

Decrease in IgE Fc receptor expression on mouse bone marrow-derived mast cells and inhibition of PAF-acether formation and of β-hexosaminidase release by dexamethasone. / Benhamou, M.; Ninio, E.; Salem, P.; Hieblot, C.; Bessou, G.; Pitton, C.; Liu, Fu-Tong; Mencia-Huerta, J. M.

In: Journal of Immunology, Vol. 136, No. 4, 1986, p. 1385-1392.

Research output: Contribution to journalArticle

Benhamou, M, Ninio, E, Salem, P, Hieblot, C, Bessou, G, Pitton, C, Liu, F-T & Mencia-Huerta, JM 1986, 'Decrease in IgE Fc receptor expression on mouse bone marrow-derived mast cells and inhibition of PAF-acether formation and of β-hexosaminidase release by dexamethasone', Journal of Immunology, vol. 136, no. 4, pp. 1385-1392.
Benhamou, M. ; Ninio, E. ; Salem, P. ; Hieblot, C. ; Bessou, G. ; Pitton, C. ; Liu, Fu-Tong ; Mencia-Huerta, J. M. / Decrease in IgE Fc receptor expression on mouse bone marrow-derived mast cells and inhibition of PAF-acether formation and of β-hexosaminidase release by dexamethasone. In: Journal of Immunology. 1986 ; Vol. 136, No. 4. pp. 1385-1392.
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abstract = "The effect of dexamethasone (DM) on the immunologic and nonimmunologic release of paf-acether and of the granule marker β-hexosaminidase (BHEX) from mouse bone marrow-derived mast cells (BMMC) was studied. BMMC (1 x 106) in a modified Tyrode's solution containing 0.25{\%} bovine serum albumin (BSA) were sensitized with an optimal dose of dinitrophenyl (DNP)-specific monoclonal IgE, and were washed before challenge with 40 ng/ml of DNP coupled to BSA. Preincubation of BMMC for 24 hr with 1 nM to 1 μM DM inhibited in a dose-dependent fashion the immunologic release of paf-acether and of BHEX as compared with control cells, with a half-maximal effect at 20 nM and 4 nM respectively. By contrast, the ionophore A23187 (1 μM)-induced release of paf-acether and of BHEX was unaffected by DM pretreatment. Finally, the antigen-induced increase in acetyltransferase activity, used as an index of cellular activation, was inhibited by 37 ± 16{\%} in 1 μM DM-treated BMMC as compared with untreated cells. Preincubation of BMMC with DM for 24 hr caused a dose-dependent inhibition of 125I-IgE binding to the cells, with a half-maximal effect at 14 nM. As determined by Scatchard analysis, the number of IgE Fc receptors was decreased by 55{\%} in 1 μM DM-treated BMMC as compared with untreated cells, although the dissociation constants were comparable (control: 12.6 ± 4.1 nM; DM-treated cells: 14.1 ± 6.7 nM; mean ± SD; n = 3). Cytofluorometer analysis of BMMC sensitized with a saturating amount of purified monoclonal IgE, followed by addition of a fluoresceinated anti-mouse IgG (heavy and light chains), revealed a single cellular population for both DM-treated and untrated BMMC. This demonstrates that the DM-induced decrease in IgE Fc receptor expression was exhibited by every BMMC. The possible link between the decreased sensitization of the cells consequent to the reduction in IgE Fc receptor expression and the alteration of the secretory response and acetyltransferase activity was investigated. BMMC were incubated with IgE under experimental conditions giving half-sensitization of the cells. Upon antigen challenge, a 10.5 ± 3.7{\%} decrease in acetyltransferase activity and a 29.2 ± 3.5{\%} decrease in paf-acether release were observed with half-sensitized cells as compared with cells sensitized with a saturating amount of IgE. This result indicates that the decreased sensitization of the cells do not fully account for the inhibitions of paf-acether release and acetyltransferase activity observed upon DM treatment. These results indicate that DM inhibits the immunologic release of paf-acether and of BHEX from passively sensitized BMMC and decreases the IgE Fc receptor number available for sensitization. Thus, the modulation of IgE Fc receptor number could explain part of the anti-allergic properties of glucocorticosteroids.",
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T1 - Decrease in IgE Fc receptor expression on mouse bone marrow-derived mast cells and inhibition of PAF-acether formation and of β-hexosaminidase release by dexamethasone

AU - Benhamou, M.

AU - Ninio, E.

AU - Salem, P.

AU - Hieblot, C.

AU - Bessou, G.

AU - Pitton, C.

AU - Liu, Fu-Tong

AU - Mencia-Huerta, J. M.

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N2 - The effect of dexamethasone (DM) on the immunologic and nonimmunologic release of paf-acether and of the granule marker β-hexosaminidase (BHEX) from mouse bone marrow-derived mast cells (BMMC) was studied. BMMC (1 x 106) in a modified Tyrode's solution containing 0.25% bovine serum albumin (BSA) were sensitized with an optimal dose of dinitrophenyl (DNP)-specific monoclonal IgE, and were washed before challenge with 40 ng/ml of DNP coupled to BSA. Preincubation of BMMC for 24 hr with 1 nM to 1 μM DM inhibited in a dose-dependent fashion the immunologic release of paf-acether and of BHEX as compared with control cells, with a half-maximal effect at 20 nM and 4 nM respectively. By contrast, the ionophore A23187 (1 μM)-induced release of paf-acether and of BHEX was unaffected by DM pretreatment. Finally, the antigen-induced increase in acetyltransferase activity, used as an index of cellular activation, was inhibited by 37 ± 16% in 1 μM DM-treated BMMC as compared with untreated cells. Preincubation of BMMC with DM for 24 hr caused a dose-dependent inhibition of 125I-IgE binding to the cells, with a half-maximal effect at 14 nM. As determined by Scatchard analysis, the number of IgE Fc receptors was decreased by 55% in 1 μM DM-treated BMMC as compared with untreated cells, although the dissociation constants were comparable (control: 12.6 ± 4.1 nM; DM-treated cells: 14.1 ± 6.7 nM; mean ± SD; n = 3). Cytofluorometer analysis of BMMC sensitized with a saturating amount of purified monoclonal IgE, followed by addition of a fluoresceinated anti-mouse IgG (heavy and light chains), revealed a single cellular population for both DM-treated and untrated BMMC. This demonstrates that the DM-induced decrease in IgE Fc receptor expression was exhibited by every BMMC. The possible link between the decreased sensitization of the cells consequent to the reduction in IgE Fc receptor expression and the alteration of the secretory response and acetyltransferase activity was investigated. BMMC were incubated with IgE under experimental conditions giving half-sensitization of the cells. Upon antigen challenge, a 10.5 ± 3.7% decrease in acetyltransferase activity and a 29.2 ± 3.5% decrease in paf-acether release were observed with half-sensitized cells as compared with cells sensitized with a saturating amount of IgE. This result indicates that the decreased sensitization of the cells do not fully account for the inhibitions of paf-acether release and acetyltransferase activity observed upon DM treatment. These results indicate that DM inhibits the immunologic release of paf-acether and of BHEX from passively sensitized BMMC and decreases the IgE Fc receptor number available for sensitization. Thus, the modulation of IgE Fc receptor number could explain part of the anti-allergic properties of glucocorticosteroids.

AB - The effect of dexamethasone (DM) on the immunologic and nonimmunologic release of paf-acether and of the granule marker β-hexosaminidase (BHEX) from mouse bone marrow-derived mast cells (BMMC) was studied. BMMC (1 x 106) in a modified Tyrode's solution containing 0.25% bovine serum albumin (BSA) were sensitized with an optimal dose of dinitrophenyl (DNP)-specific monoclonal IgE, and were washed before challenge with 40 ng/ml of DNP coupled to BSA. Preincubation of BMMC for 24 hr with 1 nM to 1 μM DM inhibited in a dose-dependent fashion the immunologic release of paf-acether and of BHEX as compared with control cells, with a half-maximal effect at 20 nM and 4 nM respectively. By contrast, the ionophore A23187 (1 μM)-induced release of paf-acether and of BHEX was unaffected by DM pretreatment. Finally, the antigen-induced increase in acetyltransferase activity, used as an index of cellular activation, was inhibited by 37 ± 16% in 1 μM DM-treated BMMC as compared with untreated cells. Preincubation of BMMC with DM for 24 hr caused a dose-dependent inhibition of 125I-IgE binding to the cells, with a half-maximal effect at 14 nM. As determined by Scatchard analysis, the number of IgE Fc receptors was decreased by 55% in 1 μM DM-treated BMMC as compared with untreated cells, although the dissociation constants were comparable (control: 12.6 ± 4.1 nM; DM-treated cells: 14.1 ± 6.7 nM; mean ± SD; n = 3). Cytofluorometer analysis of BMMC sensitized with a saturating amount of purified monoclonal IgE, followed by addition of a fluoresceinated anti-mouse IgG (heavy and light chains), revealed a single cellular population for both DM-treated and untrated BMMC. This demonstrates that the DM-induced decrease in IgE Fc receptor expression was exhibited by every BMMC. The possible link between the decreased sensitization of the cells consequent to the reduction in IgE Fc receptor expression and the alteration of the secretory response and acetyltransferase activity was investigated. BMMC were incubated with IgE under experimental conditions giving half-sensitization of the cells. Upon antigen challenge, a 10.5 ± 3.7% decrease in acetyltransferase activity and a 29.2 ± 3.5% decrease in paf-acether release were observed with half-sensitized cells as compared with cells sensitized with a saturating amount of IgE. This result indicates that the decreased sensitization of the cells do not fully account for the inhibitions of paf-acether release and acetyltransferase activity observed upon DM treatment. These results indicate that DM inhibits the immunologic release of paf-acether and of BHEX from passively sensitized BMMC and decreases the IgE Fc receptor number available for sensitization. Thus, the modulation of IgE Fc receptor number could explain part of the anti-allergic properties of glucocorticosteroids.

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