Importance of concomitant local and systemic eosinophilia in uncontrolled asthma

Abstract

reagent. Their findings further suggest that for the paucibacillary type of samples, such as CSF, less sample reagent might be necessary.These findings need to be confirmed independently and should be combined with testing of the tuberculocidal effect at lower sample-to-sample-reagent ratios before they can be recommended for clinical use. We hope that other groups will follow the example of R.F. Luo and co-workers and evaluate different protocols for different sample types, so that Xpert testing on nonrespiratory samples can be optimised. Importance of concomitant local and systemic eosinophilia in uncontrolled asthmaTo the Editor:We read with interest the comprehensive, combined retrospective and prospective study on eosinophilia in asthma by SCHLEICH et al. [1]. As compellingly demonstrated by SCHLEICH et al.[1] concomitant elevation of sputum and blood eosinophil numbers is an important factor in poorly controlled asthma. These data agree with the view that both local airway ''inflammation'' and blood eosinophilia contribute as risk factors in asthma [2]. However, there are additional eosinophil features, other than just counts, that characterise asthma. Here we draw attention to the potential roles of primary lysis/necrosis of eosinophils as blood biomarkers and bronchial-pathogenic mechanisms, especially in uncontrolled asthma.SCHLEICH et al.[1] briefly discuss previous findings on eosinophil numbers reported by VOLBEDA et al. [3]. However, a principal message of the latter study concerned association between poor asthma control and ''activated eosinophils'' and loss of ''epithelial intactness'', respectively, in bronchial biopsies. It emerged that the eosinophils had been activated by primary lysis that results in the spilling of toxic protein-releasing free eosinophil granules (FEGs) in the bronchial tissue [3,4]. 1096Furthermore, contrasting the significant associations with FEGs, poor asthma control was not associated with the number of eosinophils in sputum or bronchial tissue [3,4].The observations by VOLBEDA et al.[3] support pathogenic roles of primary eosinophil lysis-produced, release-competent FEGs. Intriguing is the potential of this mechanism to derange the epithelial lining and evoke inflammation and remodelling as a consequence of exaggerated epithelial repair [5]. Inflammation should probably be equalled to inflammatory activity rather than the number of eosinophils.MUNIZ-JUNQUEIRA et al. [6] demonstrate that blood eosinophils undergo lysis (plus spilling of FEGs) more readily the more severe the asthma is. Unprecedentedly, the pro-lysis propensity distinctly separates three levels of severity amongst children with acute asthma exacerbations [6]. Hence, proclivity of blood eosinophils for primary lysis may biomark severe asthma.Inferentially, eosinophils would be primed for cytolysis before arriving in severely diseased bronchi. Priming may be produced by interleukin (IL)-5, which switches pro-apoptosis responses into primary lysis, as reviewed in PERSSON and ULLER [7]. We think such switc...