The effect of cationic charge on release of eosinophil mediators

Adamko, Darryl J.; Wu, Yingqi; Ajamian, Farnam; Ilarraza, Ramses; Moqbel, Redwan; Gleich, Gerald J.

doi:10.1016/j.jaci.2008.03.020

Cited by 17 publications

(16 citation statements)

References 44 publications

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“…The inhibition of released EPO by 10 −6 M Wortmannin was significant in the rhinitic group compared to the controls during pollen season and after bronchial challenge. It has been postulated that the very low release values of EPO in degranulation assays depends on the sticky nature of the protein, due to a very high cationic charge with a isoelectric point of 10.8, and therefore adhering to the test tubes when investigated [39]. It has also been demonstrated that Wortmannin inhibits EPO release in vitro, possibly by blocking CD18, after incubation with a cytokine cocktail of IL-3, IL-5 and GM-CSF [39].…”

Section: Discussionmentioning

confidence: 99%

“…It has been postulated that the very low release values of EPO in degranulation assays depends on the sticky nature of the protein, due to a very high cationic charge with a isoelectric point of 10.8, and therefore adhering to the test tubes when investigated [39]. It has also been demonstrated that Wortmannin inhibits EPO release in vitro, possibly by blocking CD18, after incubation with a cytokine cocktail of IL-3, IL-5 and GM-CSF [39]. In addition, EPO has been shown to be the most potent eosinophil granule protein, on a molar basis, to kill helminths [2], and perhaps not playing an important role in allergic reactions.…”

Section: Discussionmentioning

confidence: 99%

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PI3-Kinase Regulates Eosinophil and Neutrophil Degranulation in Patients with Allergic Rhinitis and Allergic Asthma Irrespective of Allergen Challenge Model

et al. 2011

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The PI3K pathway plays a major role in many vital cell processes. Our primary aim was to investigate signalling through PI3K for in vitro degranulation from allergen-primed eosinophils and neutrophils in allergic rhinitis and allergic asthma after seasonal and experimental allergen challenge. Nine patients with allergic rhinitis, eight with allergic asthma and four controls were studied during birch pollen season and after nasal and bronchial allergen challenge. Primed blood eosinophils and neutrophils were stimulated for in vitro degranulation with C3b-coated Sephadex particles, after prior incubation with Wortmannin, a PI3K inhibitor. The released amounts of eosinophil cationic protein (ECP), eosinophil peroxidase (EPO) and myeloperoxidase (MPO) were measured by radioimmunoassay. Wortmannin (10(-6) to 10(-9) M) inhibited ECP, EPO and MPO release in a dose-dependent manner in allergic rhinitis and allergic asthma in all three allergen challenge models. Inhibition of ECP release tended to be lower in the asthmatics in all allergen challenge models, statistically significant compared to the controls during season for 10(-8) M Wortmannin (p=0.01). A clear propensity towards less inhibition in the rhinitic patients was seen after nasal and bronchial challenge compared to seasonal exposure, significant for ECP (10(-8) M Wortmannin; p=0.034 and 0.002, respectively). Signalling through PI3K is clearly involved in ECP, EPO and MPO release in allergic rhinitis and allergic asthma irrespective of allergen challenge model. Allergic asthma demonstrated less inhibition of ECP release via PI3K during pollen season, indicating that other pathways play a greater role in eosinophil degranulation in allergic asthma than allergic rhinitis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

PI3-Kinase Regulates Eosinophil and Neutrophil Degranulation in Patients with Allergic Rhinitis and Allergic Asthma Irrespective of Allergen Challenge Model

et al. 2011

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“…In mono-culture, MC were cultured at 1*10 5 /100μl, and Eos from 1*10 5 to 1*10 6 /100μl. EPO release was determined by a colorimetric assay by using a standardized assay with purified human EPO diluted in serial half-dilutions to a final concentration of 2 nM and with the peroxidase substrate solution containing o-phenylenediamine (OPD), as previously described (Adamko et al 2008). Cell samples and purified EPO were incubated in pre-coated 96-well flat plates (Nunc) for 45 min at 37°C and 5% CO 2 in a humidified atmosphere.…”

Section: Influence Of MC On Epo Release From Eosmentioning

confidence: 99%

Ultrastructural evidence for human mast cell-eosinophil interactions in vitro

et al. 2010

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We have hypothesized that mast cells (MC) and eosinophils (Eos), the main effectors of allergy, can form an effector unit. These cells co-exist in the inflamed tissues during the late and chronic stages of allergy and have been shown to be capable of influencing each other's survival and activity via soluble mediators. We have recently described couples of receptor-ligands that are expressed on either/both of these cells and that imply a physical interaction. In this study, we have investigated the existence of short-term (60 min) in vitro interactions between human peripheral blood Eos and cord-blood-derived MC by transmission electron microscopy. We have found that MC and Eos adhere to each other; the lipid body content and the granule morphology of co-cultured MC and Eos, respectively, are altered, and the level of Eos peroxidase (EPO) released by co-cultured Eos is elevated. Moreover, the transfer of EPO from Eos to MC and tryptase from MC to Eos has been observed. Our results thus indicate that, when co-cultured, MC and Eos show signs of physical contact and of reciprocal activation. This is the first in vitro evidence of functional physical interactions between human MC and Eos, interactions that might also occur in vivo during allergic diseases.

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“…Lysine-coated cyanogen bromide-coupled Sepharose beads (PharMingen, San Diego, Calif) were added (for 2 hours at 378C) to improve eosinophil mediator release. 28 Some eosinophils were preincubated with the phosphoinositide 3 (PI3)-kinase inhibitor wortmannin (Sigma-Aldrich, St Louis, Mo).…”

Section: Coculturing Of T Cells Macrophages/dendritic Cells and Virusmentioning

confidence: 99%

Virus-induced eosinophil mediator release requires antigen-presenting and CD4+ T cells

Davoine

Cao

et al. 2008

Journal of Allergy and Clinical Immunology

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The effect of cationic charge on release of eosinophil mediators

Cited by 17 publications

References 44 publications

PI3-Kinase Regulates Eosinophil and Neutrophil Degranulation in Patients with Allergic Rhinitis and Allergic Asthma Irrespective of Allergen Challenge Model

PI3-Kinase Regulates Eosinophil and Neutrophil Degranulation in Patients with Allergic Rhinitis and Allergic Asthma Irrespective of Allergen Challenge Model

Ultrastructural evidence for human mast cell-eosinophil interactions in vitro

Virus-induced eosinophil mediator release requires antigen-presenting and CD4+ T cells

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