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Dissecting the role of eosinophil cationic protein in upper airway disease

Bystrom, Jonas; Patel, Smita Y.; Amin, Kawa; Bishop-Bailey, David

Current Opinion in Allergy and Clinical Immunology: February 2012 - Volume 12 - Issue 1 - p 18–23
doi: 10.1097/ACI.0b013e32834eccaf
RHINITIS, SINUSITIS AND UPPER AIRWAY DISEASE: Edited by Ruby Pawankar and David P. Skoner

Purpose of review Eosinophil granulocyte myeloid cells are increased in atopic and nonatopic rhinitis, chronic rhinosinusitis (CRS) and atopic keratoconjunctivitis, diseases of the upper respiratory tract. Eosinophils contain several basic granule proteins, the best known being the eosinophil cationic protein (ECP). ECP is a cytotoxic, pro-fibrotic ribonuclease, which is found deposited in these eosinophil-related diseases and is often used in parallel with blood eosinophilia to monitor those diseases. The contribution of eosinophils and their granule proteins to disease pathogenesis have been debated; recent findings might bring these cells to the center of attention.

Recent findings Novel mediators of atopic disease, interleukin-17 (IL-17) and IL-33 have been found in the upper respiratory tract. These cytokines stimulate eosinophils to survival and degranulation, IL-17 via granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-33 directly. Transforming growth factor (TGF)-β has been found in CRS and atopic keratoconjunctivitis mucosa, its production possibly stimulated by ECP. ECP is detected in nasal mucosa of local allergic reactions, entopy, in rhinitis and CRS. ECP might be released from freely circulating eosinophil granules or in association with eosinophil mitochondrial DNA, both means of release for pathogen defence.

Summary Novel evidence suggests that eosinophils and ECP might have new prominent roles in development of diseases of the upper respiratory tract.

aBone and Joint Research Unit, William Harvey Research Institute, Barts and The London, Queen Mary University of London, London

bNuffield Department of Medicine, Oxford University, Level 5, John Radcliffe Hospital, Oxford, UK

cRespiratory Medicine and Allergology Unit, Department of Medical Science, Uppsala University Hospital, Uppsala, Sweden

dDepartment of Microbiology/Immunology, Faculty of Medical Science, University of Sulaimani, Sulaimani, Iraq

eDepartment of Translation Medicine and Therapeutics, William Harvey Research Institute, Barts and The London, Queen Mary University of London, London, UK

Correspondence to Jonas Bystrom, PhD, Bone and Joint Research Unit, William Harvey Research Institute, Barts and The London, Queen Mary University of London, London, EC1M 6BQ, UK. Tel: +44 20 7882 2473; e-mail: j.bystrom@qmul.ac.uk

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