Abstract
Two recent articles by the same research group documented that patients with severe eosinophilic asthma exhibit an increased proportion of a subtype of eosinophils, namely CD62Llow inflammatory eosinophils (iEos) and identified an intriguing correlation between such iEos and asthma control scores. Moreover, CD62Llow iEos were reduced after treatment with the anti-IL-5 monoclonal antibody mepolizumab. In the future, we believe that eosinophil subtypes could represent a useful biomarker in severe eosinophilic asthma, helping clinicians characterize patient endotypes and monitoring the response to biological drugs.
Tweetable abstract
Patients with severe eosinophilic asthma (SEA) have an increased proportion of a subtype of eosinophils, CD62Llow inflammatory eosinophils (iEos), which are reduced after mepolizumab treatment. iEos might represent a novel useful biomarker in SEA.
Summary of materials & methods
Discussion & conclusion
In particular, iEos seem to be present in patients with severe eosinophilic asthma (SEA) in a higher proportion when compared with healthy subjects and mild asthmatic patients, although evidence is still contrasting.
The iEos proportion seems not to be significantly affected by oral corticosteroids (albeit their value was numerically higher in this subgroup of patients), correlating with symptom severity assessed through the Asthma Control Test and Asthma Control Questionnaire 5.
iEos might be a novel biomarker of SEA.
Future perspectives
Novel studies are needed to ascertain whether iEos and resident eosinophils could be affected by other biological drugs licensed for SEA, and whether iEos could be specifically targeted by newly developed drugs.
Novel studies might focus on eosinophilic inflammation in medical conditions other than SEA, such as eosinophilic granulomatosis with polyangiitis and eosinophilic esophagitis.
The prevalence of iEos in mild-to-moderate asthma is still unclear, and therefore research should be done in order to ascertain whether iEos might be useful to discriminate asthma severity.
Author contributions
C Candia and M Maniscalco conceived and designed the study, interpreted results and drafted the manuscript. C Candia, M Maniscalco, S D’Anna and P Ambrosino interpreted results and performed critical revisions. C Candia, A Motta and M Maniscalco drafted the manuscript and performed critical revisions. M Maniscalco, A Motta and P Ambrosino supervised the project, interpreted results and drafted the manuscript. All authors read and approved the final version of the manuscript.
Financial disclosure
This work was partially supported by the ‘Ricerca Corrente’ funding scheme of the Ministry of Health, Italy. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Competing interests disclosure
The authors have no competing interests or relevant affiliations with any organization or entity with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, stock ownership or options and expert testimony.
Writing disclosure
No writing assistance was utilized in the production of this manuscript.