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Effects of dexamethasone on TNF-alpha-induced release of cytokines from purified human blood eosinophils.

Uings I, Puxeddu I, Temkin V, Smith SJ, Fattah D, Ray KP, Levi-Schaffer F - Clin Mol Allergy (2005)

Bottom Line: METHODS: The effect of dexamethasone on TNF-alpha induced eosinophils survival, degranulation (ECP), cytokines release (IL-8, GM-CSF) and adhesion to VCAM-1, ICAM-1 and IgG coated wells (EPO release) were evaluated.RESULTS: The drug inhibited IL-8 and GM-CSF production, but not viability, degranulation or adhesion in human peripheral blood eosinophils.CONCLUSION: These results indicate that part of the activity of glucocorticosteroids on eosinophils may be mediated by their ability to inhibit cytokine secretion that in turn is important for the perpetuation of the allergic inflammation.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pharmacology, School of Pharmacy, The Hebrew University of Jerusalem, Jerusalem, Israel. fls@cc.huji.ac.il.

ABSTRACT
SUMMARY: BACKGROUND: TNF-alpha is an important mediator in allergy also for its effects on eosinophils. METHODS: The effect of dexamethasone on TNF-alpha induced eosinophils survival, degranulation (ECP), cytokines release (IL-8, GM-CSF) and adhesion to VCAM-1, ICAM-1 and IgG coated wells (EPO release) were evaluated. RESULTS: The drug inhibited IL-8 and GM-CSF production, but not viability, degranulation or adhesion in human peripheral blood eosinophils. CONCLUSION: These results indicate that part of the activity of glucocorticosteroids on eosinophils may be mediated by their ability to inhibit cytokine secretion that in turn is important for the perpetuation of the allergic inflammation.

No MeSH data available.


Related in: MedlinePlus

Effect of TNF-α on IL-8 release from eosinophils. Eosinophils were cultured with different concentrations of TNF-α (0 – 100 ng/ml). IL-8 release was evaluated by ELISA. Values are mean ± SEM (n = 5).
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Figure 3: Effect of TNF-α on IL-8 release from eosinophils. Eosinophils were cultured with different concentrations of TNF-α (0 – 100 ng/ml). IL-8 release was evaluated by ELISA. Values are mean ± SEM (n = 5).

Mentions: Incubation of eosinophils with TNF-α induced a significant release of ECP compared to eosinophils cultured in medium alone (24.5 ± 8.9 vs 6.9 ± 1.2 pg/106; p < 0.05). However, addition of dexamethasone in the cultures did not affect TNF-α-induced ECP release (Figure 2). The release of IL-8 by TNF-α treated eosinophils was dose-dependently proportional to the concentrations of TNF-α. A maximal release was achieved at 100 ng/ml (1770,49 ± 129 pg/ml; p < 0.05) (Figure 3). TNF-α also induced GM-CSF release by eosinophils although to a lesser extent than that of IL-8 (data not shown). Treatment of the cultures with dexamethasone completely blocked the TNF-α-induced release of both IL-8 and GM-CSF (p < 0.05) (Figures 4A–B). TNF-α enhanced significantly the percentage of eosinophil adhesion to VCAM-1, ICAM-1 and IgG in comparison to medium alone, by 177%, 205% and 169%, respectively. However, this effect was not inhibited by dexamethasone (Figure 5).


Effects of dexamethasone on TNF-alpha-induced release of cytokines from purified human blood eosinophils.

Uings I, Puxeddu I, Temkin V, Smith SJ, Fattah D, Ray KP, Levi-Schaffer F - Clin Mol Allergy (2005)

Effect of TNF-α on IL-8 release from eosinophils. Eosinophils were cultured with different concentrations of TNF-α (0 – 100 ng/ml). IL-8 release was evaluated by ELISA. Values are mean ± SEM (n = 5).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC1131914&req=5

Figure 3: Effect of TNF-α on IL-8 release from eosinophils. Eosinophils were cultured with different concentrations of TNF-α (0 – 100 ng/ml). IL-8 release was evaluated by ELISA. Values are mean ± SEM (n = 5).
Mentions: Incubation of eosinophils with TNF-α induced a significant release of ECP compared to eosinophils cultured in medium alone (24.5 ± 8.9 vs 6.9 ± 1.2 pg/106; p < 0.05). However, addition of dexamethasone in the cultures did not affect TNF-α-induced ECP release (Figure 2). The release of IL-8 by TNF-α treated eosinophils was dose-dependently proportional to the concentrations of TNF-α. A maximal release was achieved at 100 ng/ml (1770,49 ± 129 pg/ml; p < 0.05) (Figure 3). TNF-α also induced GM-CSF release by eosinophils although to a lesser extent than that of IL-8 (data not shown). Treatment of the cultures with dexamethasone completely blocked the TNF-α-induced release of both IL-8 and GM-CSF (p < 0.05) (Figures 4A–B). TNF-α enhanced significantly the percentage of eosinophil adhesion to VCAM-1, ICAM-1 and IgG in comparison to medium alone, by 177%, 205% and 169%, respectively. However, this effect was not inhibited by dexamethasone (Figure 5).

Bottom Line: METHODS: The effect of dexamethasone on TNF-alpha induced eosinophils survival, degranulation (ECP), cytokines release (IL-8, GM-CSF) and adhesion to VCAM-1, ICAM-1 and IgG coated wells (EPO release) were evaluated.RESULTS: The drug inhibited IL-8 and GM-CSF production, but not viability, degranulation or adhesion in human peripheral blood eosinophils.CONCLUSION: These results indicate that part of the activity of glucocorticosteroids on eosinophils may be mediated by their ability to inhibit cytokine secretion that in turn is important for the perpetuation of the allergic inflammation.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pharmacology, School of Pharmacy, The Hebrew University of Jerusalem, Jerusalem, Israel. fls@cc.huji.ac.il.

ABSTRACT
SUMMARY: BACKGROUND: TNF-alpha is an important mediator in allergy also for its effects on eosinophils. METHODS: The effect of dexamethasone on TNF-alpha induced eosinophils survival, degranulation (ECP), cytokines release (IL-8, GM-CSF) and adhesion to VCAM-1, ICAM-1 and IgG coated wells (EPO release) were evaluated. RESULTS: The drug inhibited IL-8 and GM-CSF production, but not viability, degranulation or adhesion in human peripheral blood eosinophils. CONCLUSION: These results indicate that part of the activity of glucocorticosteroids on eosinophils may be mediated by their ability to inhibit cytokine secretion that in turn is important for the perpetuation of the allergic inflammation.

No MeSH data available.


Related in: MedlinePlus