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Review

Human Eosinophil Innate Response to Alternaria Fungus through Protease-Activated Receptor-2

Matsuwaki Y.a, b · Wada K.a, b · Moriyama H.a · Kita H.b

Author affiliations

aDepartment of Otorhinolaryngology, The Jikei University School of Medicine, Tokyo, Japan; bDepartments of Immunology and Medicine, Mayo Clinic, Rochester, Minn., USA

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Int Arch Allergy Immunol 2011;155(suppl 1):123–128

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Article / Publication Details

First-Page Preview
Abstract of Review

Published online: June 01, 2011
Issue release date: June 2011

Number of Print Pages: 6
Number of Figures: 1
Number of Tables: 0

ISSN: 1018-2438 (Print)
eISSN: 1423-0097 (Online)

For additional information: https://www.karger.com/IAA

Abstract

Eosinophils are multifunctional leukocytes implicated in the pathogenesis of allergic diseases. An association between eosinophilic inflammation and infection or colonization by fungi has also been long recognized. However, the mechanisms underlying how eosinophils are activated and how they release proinflammatory and immunomodulatory mediators such as major basic protein (MBP) and eosinophil-derived neurotoxin remain largely unknown. We used a fungus, i.e. Alternaria, as a model microbe relevant to human asthma and chronic rhinosinusitis (CRS) to investigate the molecular mechanisms involved in the immune recognition of ubiquitous environmental allergens. Human eosinophils are activated by live Alternaria alternata organisms, release their granule proteins, and kill the fungi. Eosinophils, but not neutrophils, respond to secreted products from A. alternata. We found that eosinophils are equipped with innate cellular activation machinery that responds to an extracellular aspartate protease secreted by Alternaria. Aspartate protease activation of protease-activated receptor (PAR)-2 probably involves a novel mechanism different from that for serine protease activation of PAR-2. Thus, human eosinophils may recognize certain danger signals or virulence factors produced by fungi and provoke inflammatory responses against these organisms. Dysregulation of such an innate immune mechanism may be involved in the pathophysiology of certain human inflammatory diseases, including asthma and CRS.

© 2011 S. Karger AG, Basel


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Article / Publication Details

First-Page Preview
Abstract of Review

Published online: June 01, 2011
Issue release date: June 2011

Number of Print Pages: 6
Number of Figures: 1
Number of Tables: 0

ISSN: 1018-2438 (Print)
eISSN: 1423-0097 (Online)

For additional information: https://www.karger.com/IAA


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