Differential inhibition of inflammatory effector functions by petasin, isopetasin and neopetasin in human eosinophils

@article{Thomet2001DifferentialIO,
  title={Differential inhibition of inflammatory effector functions by petasin, isopetasin and neopetasin in human eosinophils},
  author={Olivier A. R. Thomet and Ulrich N. Wiesmann and Kurt Blaser and Hans-Uwe Simon},
  journal={Clinical \& Experimental Allergy},
  year={2001},
  volume={31}
}
Background Priming of eosinophils with granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) and subsequent stimulation with platelet‐activating factor (PAF) or the anaphylatoxin C5a is associated with a rapid production of leukotrienes (LTs) and release of eosinophil cationic protein (ECP). 
Anti‐inflammatory effects of the petasin phyto drug Ze339 are mediated by inhibition of the STAT pathway
TLDR
The study uncovers Ze339 modulated changes in pro-inflammatory mediators and decreased neutrophil chemotaxis as well as a reduction of the nuclear translocation and phosphorylation of STAT molecules, suggesting that phyto drug Ze339 specifically targets STAT-signalling pathways in HNECs and has high potential as a broad anti-inflammatory drug that exceeds current indication. Expand
Petasites extract Ze 339 (PET) inhibits allergen‐induced Th2 responses, airway inflammation and airway hyperreactivity in mice
Background: The herbal Petasites hybridus (butterbur) extract (Ze 339, PET) is known to have leukotriene inhibiting properties, and therefore might inhibit allergic diseases.
Neutrophil apoptosis mediated by nicotinic acid receptors (GPR109A)
TLDR
It is demonstrated that mature human neutrophils, but not eosinophils, express functional GPR109A receptors, which might be involved in the regulation of neutrophil numbers. Expand
Anti-inflammatory activity of an extract of Petasites hybridus in allergic rhinitis.
TLDR
The results suggest that Ze339 is effective in treating allergic rhinitis patients by decreasing levels of nasal inflammatory mediators and quality-of-life scores significantly improved. Expand
Effects of intranasal corticosteroid on nasal adenosine monophosphate challenge in persistent allergic rhinitis *
TLDR
Response to a single dose nasal adenosine monophosphate challenge has been used as a surrogate inflammatory marker for allergic rhinitis and receipt of response following intranasal corticosteroid would validate the challenge. Expand
Chapter 12 – Eosinophils
TLDR
Since eosinophils exhibit a multifunctional role in the pathogenesis of asthma, therapeutic approaches aiming to reduce their numbers and/or activity seem promising. Expand
Butterbur, a herbal remedy, attenuates adenosine monophosphate induced nasal responsiveness in seasonal allergic rhinitis
Background Butterbur (BB) or Petasites hybridus, a herbal remedy, exhibits in vitro inhibition of cysteinyl leukotriene biosynthesis. However, no placebo‐controlled studies have been performed toExpand
Petasins in the Treatment of Allergic Diseases: Results of Preclinical and Clinical Studies
TLDR
The clinical efficacy of the butterbur extract drug was compared with an established antihistamine treatment scheme in a double-blind study and no significant difference was observed between the two treatment groups. Expand
The potential of natural products as effective treatments for allergic inflammation: implications for allergic rhinitis.
  • M. Kulka
  • Medicine
  • Current topics in medicinal chemistry
  • 2009
TLDR
The molecular mechanisms and scientific validity of some herbal remedies currently used clinically in the treatment of allergic rhinitis will be explored and mast cells and their mediators are focused on. Expand
The anti‐migraine component of butterbur extracts, isopetasin, desensitizes peptidergic nociceptors by acting on TRPA1 cation channel
TLDR
The ability of isopetasin, a major constituent of extracts of butterbur, to specifically target TRPA1 channel and to affect functional responses relevant to migraine is investigated. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 48 REFERENCES
ERK1 and ERK2 Activation by Chemotactic Factors in Human Eosinophils Is Interleukin 5-dependent and Contributes to Leukotriene C4 Biosynthesis*
TLDR
Evidence is provided for a previously undescribed fundamental mechanism by which stimulation of IL-5 family receptors induces a rapid phenotypic alteration in the signal transduction pathways of chemotactic receptors, enabling their activation of the ERK1 and ERK2 pathway and contributing to the capacity of these cells to synthesize LTC4. Expand
GM-CSF regulates human eosinophil responses to F-Met peptide and platelet activating factor.
TLDR
It is concluded that expression of adherence molecules, transmembrane signaling, and adherence responses of eosinophils are enhanced by exposure to GM-CSF, which could potentiate the adherence to endothelium and subsequent migration of eanophils to inflammatory sites in vivo. Expand
Regulatory effect of cytokines on eosinophil degranulation.
TLDR
It is suggested that cytokines which induce eosinophil differentiation and proliferation during hematopoiesis also enhance the effector function of mature eOSinophils and that IFN-gamma partially down-regulates eos inophil degranulation. Expand
Eotaxin induces degranulation and chemotaxis of eosinophils through the activation of ERK2 and p38 mitogen-activated protein kinases.
TLDR
It is concluded that eotaxin induces a rapid concentration-dependent activation of ERK2 and p38 in eosinophils and that the activation of these MAP kinases is required for eOTaxin-stimulated degranulation and directed locomotion. Expand
Leukotrienes and other products of the 5-lipoxygenase pathway. Biochemistry and relation to pathobiology in human diseases.
TLDR
Since the chemical characterization of the slow-reacting substance of anaphylaxis as several cysteinyl leukotrienes and the identification and biochemical assessment of the enzymes in the 5-lipoxygenase pathway, the products of this pathway have been implicated in a much broader variety of functions. Expand
Leukotriene production in human neutrophils primed by recombinant human granulocyte/macrophage colony-stimulating factor and stimulated with the complement component C5A and FMLP as second signals
TLDR
It is shown that the synthesis of lipoxygenase metabolites from endogeneous AA can be initiated in PMN through receptor mediated processes by the appropriately timed combination of biological soluble inflammatory mediator peptides and that GM-CSF not only enhances effector cell functions but can qualitatively change the mediator profile formed after activation with a second triggering signal. Expand
Interleukin-5 selectively enhances the chemotactic response of eosinophils obtained from normal but not eosinophilic subjects.
TLDR
The observed refractoriness of eos inophils from eosinophilic subjects to both directional migratory and priming effects of IL-5 in vitro, may reflect a deactivation process resulting from prior exposure in vivo. Expand
Eosinophils Maintain Their Capacity to Signal and Release Eosinophil Cationic Protein Upon Repetitive Stimulation with the Same Agonist1
TLDR
It is shown that eosinophils maintain their capacity to degranulate upon repetitive stimulation with the same agonist as long as the receptor is not occupied from a previous stimulation, implying that mature eos inophils may not require a significant ECP resynthesis. Expand
IL-5 increases expression of 5-lipoxygenase-activating protein and translocates 5-lipoxygenase to the nucleus in human blood eosinophils.
TLDR
IL-5 increases FLAP expression and translocates 5-LO to the nucleus in normal blood eosinophils in vitro, associated with an enhanced capacity for cysteinyl-leukotriene synthesis and mimics in vivo increases inFLAP expression in eos inophils from allergic asthmatics. Expand
IL-3 and IL-5 prime normal human eosinophils to produce leukotriene C4 in response to soluble agonists.
TLDR
IL-3 and IL-5 profoundly modulate the production of lipid mediators by Eos in response to the soluble agonists FMLP, C5a, and PAF, and this data further support the importance of these cytokines in inflammatory reactions involving Eos. Expand
...
1
2
3
4
5
...