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Primary lysis of eosinophils in severe desquamative asthma
Author(s) -
Persson C.
Publication year - 2014
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/cea.12255
Subject(s) - eosinophil , asthma , sputum , medicine , immunology , eosinophilia , eosinophil cationic protein , pathology , tuberculosis
Summary Primary lysis of eosinophils liberates free eosinophil granules ( FEG s) releasing toxic proteins in association with bronchial epithelial injury repair. Eosinophil lysis may be significantly pathogenic. Bronchial mucosal FEG s are associated with uncontrolled asthma, severe asthma, aspirin‐sensitive asthma, and lethal asthma. FEG s in the bronchial wall may characterize severe asthma without sputum eosinophilia. Excessive numbers of sputum FEG s occur in severe exacerbations of asthma and are reduced along with clinical improvement. Occurrence of FEG s affects interpretation of other sputum biomarkers including numbers of eosinophils, ECP , and eosinophil‐stained macrophages. Thus, eosinophil lysis produces FEG s as bronchial biomarkers of severe asthma. Blood eosinophils in severe asthma seem primed exhibiting a propensity to lyse that is greater the more severe the asthma. Proclivity of blood eosinophils to lyse also distinguished three levels of severity among children with exacerbations of asthma. Numerous FEG s releasing toxic proteins occur in association with grave derangement and shedding of epithelium in severe asthma. Subepithelial FEG s correlate negatively with intact bronchial epithelium in clinically uncontrolled asthma. Significant correlations between sputum ECP , Creola bodies, and severity of asthma exacerbations have also been demonstrated. Hence, eosinophil lysis apparently causes epithelial desquamation in severe asthma. Exaggerated epithelial repair in turn would contribute to inflammatory and remodelling features of severe asthma. Perseverance of FEG s together with maintained disease activity, despite treatment with ‘eosinophil‐depleting’ steroids and anti‐ IL 5 biologicals, agrees with the possibility that eosinophil lysis is worthy target for novel anti‐asthma drugs. Priming and lysis of eosinophils, and protein release from FEG s, are regulated and can be targeted. Eosinophil lysis and FEG s belong to the disease picture of severe asthma and need consideration in asthma studies concerned with phenotypes, biomarkers, roles of epithelial injury/repair, and targeting novel drugs.