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PI3-Kinase Regulates Eosinophil and Neutrophil Degranulation in Patients with Allergic Rhinitis and Allergic Asthma Irrespective of Allergen Challenge Model
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology. (Asthma Research Centre)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. (Gastroenterology Research Group, Asthma Research Centre)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. (Gastroenterology Research Group, Asthma Research Centre)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology. (Asthma Research Centre)
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2012 (English)In: Inflammation, ISSN 0360-3997, E-ISSN 1573-2576, Vol. 35, no 1, 230-239 p.Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2012. Vol. 35, no 1, 230-239 p.
Keyword [en]
Eosinophil inflammation, allergic rhinitis, allergic asthma, eosinophil degranulation, PI3K, ECP
National Category
Respiratory Medicine and Allergy
Research subject
Lung Medicine
Identifiers
URN: urn:nbn:se:uu:diva-131539DOI: 10.1007/s10753-011-9309-5ISI: 000300550900027OAI: oai:DiVA.org:uu-131539DiVA: diva2:354874
Available from: 2010-10-05 Created: 2010-10-04 Last updated: 2017-12-12Bibliographically approved

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Kämpe, MaryLampinen, MariaStolt, IngridJanson, ChristerStålenheim, GunnemarCarlson, Marie

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Kämpe, MaryLampinen, MariaStolt, IngridJanson, ChristerStålenheim, GunnemarCarlson, Marie
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Respiratory Medicine and AllergologyDepartment of Medical Sciences
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Inflammation
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