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Primary lysis of eosinophils in severe desquamative asthma.

Persson, Carl LU (2014) In Clinical and Experimental Allergy 44(2). p.173-183
Abstract
Primary lysis of eosinophils liberates free eosinophil granules (FEGs) releasing toxic proteins in association with bronchial epithelial injury-repair. Eosinophil lysis may be significantly pathogenic. Bronchial mucosal FEGs are associated with uncontrolled asthma, severe asthma, aspirin-sensitive asthma, and lethal asthma. FEGs in the bronchial wall may characterize severe asthma without sputum eosinophilia. Excessive numbers of sputum FEGs occur in severe exacerbations of asthma and are reduced along with clinical improvement. Occurrence of FEGs affects interpretation of other sputum biomarkers including numbers of eosinophils, ECP, and eosinophil-stained macrophages. Thus, eosinophil lysis produces FEGs as bronchial biomarkers of severe... (More)
Primary lysis of eosinophils liberates free eosinophil granules (FEGs) releasing toxic proteins in association with bronchial epithelial injury-repair. Eosinophil lysis may be significantly pathogenic. Bronchial mucosal FEGs are associated with uncontrolled asthma, severe asthma, aspirin-sensitive asthma, and lethal asthma. FEGs in the bronchial wall may characterize severe asthma without sputum eosinophilia. Excessive numbers of sputum FEGs occur in severe exacerbations of asthma and are reduced along with clinical improvement. Occurrence of FEGs affects interpretation of other sputum biomarkers including numbers of eosinophils, ECP, and eosinophil-stained macrophages. Thus, eosinophil lysis produces FEGs 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 amongst children with exacerbations of asthma. Numerous FEGs releasing toxic proteins occur in association with grave derangement and shedding of epithelium in severe asthma. Subepithelial FEGs 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 FEGs together with maintained disease activity, despite treatment with 'eosinophil-depleting' steroids and anti-IL5 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 FEGs, are regulated and can be targeted. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Clinical and Experimental Allergy
volume
44
issue
2
pages
173 - 183
publisher
Wiley-Blackwell
external identifiers
  • wos:000329926800005
  • pmid:24330324
  • scopus:84892757972
ISSN
1365-2222
DOI
10.1111/cea.12255
language
English
LU publication?
yes
id
d1973803-abb1-4e42-ba36-79b9a60df26a (old id 4223901)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24330324?dopt=Abstract
date added to LUP
2014-01-04 12:40:23
date last changed
2017-01-15 03:18:40
@article{d1973803-abb1-4e42-ba36-79b9a60df26a,
  abstract     = {Primary lysis of eosinophils liberates free eosinophil granules (FEGs) releasing toxic proteins in association with bronchial epithelial injury-repair. Eosinophil lysis may be significantly pathogenic. Bronchial mucosal FEGs are associated with uncontrolled asthma, severe asthma, aspirin-sensitive asthma, and lethal asthma. FEGs in the bronchial wall may characterize severe asthma without sputum eosinophilia. Excessive numbers of sputum FEGs occur in severe exacerbations of asthma and are reduced along with clinical improvement. Occurrence of FEGs affects interpretation of other sputum biomarkers including numbers of eosinophils, ECP, and eosinophil-stained macrophages. Thus, eosinophil lysis produces FEGs 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 amongst children with exacerbations of asthma. Numerous FEGs releasing toxic proteins occur in association with grave derangement and shedding of epithelium in severe asthma. Subepithelial FEGs 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 FEGs together with maintained disease activity, despite treatment with 'eosinophil-depleting' steroids and anti-IL5 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 FEGs, are regulated and can be targeted.},
  author       = {Persson, Carl},
  issn         = {1365-2222},
  language     = {eng},
  number       = {2},
  pages        = {173--183},
  publisher    = {Wiley-Blackwell},
  series       = {Clinical and Experimental Allergy},
  title        = {Primary lysis of eosinophils in severe desquamative asthma.},
  url          = {http://dx.doi.org/10.1111/cea.12255},
  volume       = {44},
  year         = {2014},
}