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* Department of Immunology and
Department of Medicine, Division of Allergic Disease, Mayo Graduate School, Mayo Clinic, Rochester, MN 55905;
Department of Clinical Otolaryngology, University at Buffalo, The State University of New York, Buffalo, NY 14209; and
Virginia Bioinformatics Institute, Virginia Polytechnic Institute and State University, Blacksburg, VA 24060
Eosinophils produce and release various proinflammatory mediators and also show immunomodulatory and tissue remodeling functions; thus, eosinophils may be involved in the pathophysiology of asthma and other eosinophilic disorders as well as host defense. Several major questions still remain. For example, how do human eosinophils become activated in diseased tissues or at the site of an immune response? What types of host immunity might potentially involve eosinophils? Herein, we found that human eosinophils react vigorously to a common environmental fungus, Alternaria alternata, which is implicated in the development and/or exacerbation of human asthma. Eosinophils release their cytotoxic granule proteins, such as eosinophil-derived neurotoxin and major basic protein, into the extracellular milieu and onto the surface of fungal organisms and kill the fungus in a contact-dependent manner. Eosinophils use their versatile β2 integrin molecule, CD11b, to adhere to a major cell wall component, β-glucan, but eosinophils do not express other common fungal receptors, such as dectin-1 and lactosylceramide. The I-domain of CD11b is distinctively involved in the eosinophils’ interaction with β-glucan. Eosinophils do not react with another fungal cell wall component, chitin. Because human eosinophils respond to and kill certain fungal organisms, our findings identify a previously unrecognized innate immune function for eosinophils. This immune response by eosinophils may benefit the host, but, in turn, it may also play a role in the development and/or exacerbation of eosinophil-related allergic human diseases, such as asthma.
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1 This work was supported by National Institutes of Health Grants AI34486 and AI49235 and the Mayo Foundation.
2 Address correspondence and reprint requests to Dr. Hirohito Kita, Department of Immunology and Department of Medicine, Division of Allergic Disease, Guggenheim 4, Mayo Clinic, 200 First Street SW, Rochester, MN 55095. E-mail address: kita.hirohito{at}mayo.edu
3 Abbreviations used in this paper: MBP, major basic protein; CS, calf serum; DC, dendritic cell; ECP, eosinophil cationic protein; EDN, eosinophil-derived neurotoxin; MPO, myeloperoxidase; PI, propidium iodide; RT, room temperature.
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