Cytokines modulate IgE-mediated histamine liberation from human basophils

Kristensen, K. S.; Bendtzen, Klaus; Norn, S.; Skov, Per Stahl; Pedersen, Michael; Permin, Henrik

doi:10.1007/bf01997346

Cited by 7 publications

(4 citation statements)

References 9 publications

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“…Histamine releases from the same experiments are shown in Figure 5B. In accordance with previous publications [19][20][21][22][23], IL-3 was a relatively weak activator of basophil histamine release by itself but at low concentrations (Յ10 ng/mL) led to considerable enhancement of anti-IgE-induced histamine release. Moreover, these results provide further evidence that ERK activation is not directly involved in basophil degranulation because the magnitude of ERK activity (e.g., comparing anti-IgE-stimulated with IL-3-stimulated cells) did not correlate with the percent histamine release from the cells.…”

Section: Erk-1 and -2 Activation In Basophils By Anti-ige Is Enhancedsupporting

confidence: 89%

“…However, our data also show that activation of ERK-2 is only partially responsible for arachidonic acid metabolism because IL-3, although strongly activating ERK-1 and -2, does not lead to LTC 4 production by itself. It has long been appreciated that IL-3 as well as IL-5 and granulocytemacrophage colony-stimulating factor (which all have common receptor components) can activate basophils, albeit at high concentrations (100 ng/mL) [19][20][21][22][23]. More important, however, is the fact that low concentrations (0.1-10 ng/mL) of these cytokines, which do not elicit significant histamine or LTC 4 release by themselves, can considerably enhance IgEdependent activation and LTC 4 release.…”

Section: Discussionmentioning

confidence: 99%

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Inhibitors of PI 3-kinase and MEK kinase differentially affect mediator secretion from immunologically activated human basophils

Gibbs

Grabbe

1999

Journal of Leukocyte Biology

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Effects of inhibitors of PI 3-kinase and MEK kinases were investigated on histamine, leukotriene C 4 (LTC 4 ), and cytokine release from human basophils stimulated with anti-IgE. The PI 3-kinase antagonists wortmannin (G10 nM) and LY 294002 (G1 M) strongly inhibited anti-IgE-induced release of all mediators by 40-100%. This was contrasted by the effects of the MEK kinase inhibitor PD 098059, which weakly inhibited histamine, interleukin (IL)-4, and IL-13 release but was substantially more efficacious at blocking LTC 4 production (G70% at 10 M). Previous studies have shown that arachidonic acid synthesis is controlled by MEK kinases. We observed that wortmannin, LY 294002, and PD 098059 reduce basophil ERK-1,2 activation, thus implying that, with regard to arachidonic acid metabolism, MEK kinases are a downstream target for PI-3-kinase. Our results demonstrate a universal regulatory role played by PI 3-kinases in basophil mediator production and release, whereas MEK kinase signaling is largely limited to controlling arachidonic acid metabolism.

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Section: Erk-1 and -2 Activation In Basophils By Anti-ige Is Enhancedsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Inhibitors of PI 3-kinase and MEK kinase differentially affect mediator secretion from immunologically activated human basophils

Gibbs

Grabbe

1999

Journal of Leukocyte Biology

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“…In vivo, IgE-dependent basophil activation is crucially regulated by IL-3 and GM-CSF which, at low concentrations, enhance IgE-dependent basophil activation without inducing degranulation [3]. Furthermore, priming by these cytokines transforms IgE-mediated signalling to a less calcium dependent route [5].…”

Section: Resultsmentioning

confidence: 99%

“…We have recently demonstrated that ambroxol dose-dependently inhibits the release of histamine, LTC 4 , IL-4 and IL-13 from basophils stimulated with anti-IgE (paper submitted). However, IgEdependent basophil activation is modulated in vivo by priming cytokines, such as IL-3 and GM-CSF [3]. Additionally, mediator release may also occur with non-immunological secretagogues, such as fMLP or calcium ionophores.…”

Section: Introductionmentioning

confidence: 99%

Effects of free radical scavengers on histamine release from human basophils stimulated by immunological and non-immunological secretagogues

Gibbs

Wolff

Grabbe

1999

Inflammation Research

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Fig. 1. Inhibition of IgE-dependent histamine release from human basophils by ambroxol, NAC or vitamin E. Basophils were preincubated with the drugs for 15 min either in the presence of IL-3 (1 ng/ml), GM-CSF (1 ng/ml) or buffer before stimulation with anti-IgE (1/50000 dilution). Net control releases in the absence of the drugs were 21.9 ± 7.5 % for anti-IgE alone, 33.6 ± 6.3 % for anti-IgE + IL-3 and 33.0 ± 6.4 % for anti-IgE + GM-CSF. Values are expressed as mean inhibition of control release ± SEM, n = 4. * p < 0.05 compared to control releases (paired Student's t-test).

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Granulocyte-macrophage colony-stimulating factor enhances basophil histamine release induced by non-IgE-dependent stimulators

et al. 1993

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Cytokines modulate IgE-mediated histamine liberation from human basophils

Cited by 7 publications

References 9 publications

Inhibitors of PI 3-kinase and MEK kinase differentially affect mediator secretion from immunologically activated human basophils

Inhibitors of PI 3-kinase and MEK kinase differentially affect mediator secretion from immunologically activated human basophils

Effects of free radical scavengers on histamine release from human basophils stimulated by immunological and non-immunological secretagogues

Granulocyte-macrophage colony-stimulating factor enhances basophil histamine release induced by non-IgE-dependent stimulators

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