ResearchPad - asthma-and-lower-airway-disease Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[Sputum microbiomic clustering in asthma and chronic obstructive pulmonary disease reveals a <i>Haemophilus</i>‐predominant subgroup]]> Sputum microbiomic cluster analysis and TDA demonstrates 2 subgroups of stable severe asthma and moderate‐to‐severe COPD differentiated according to dominance of Haemophilus. The Haemophilus‐high group had no defining clinical characteristics but had lower microbial diversity and increased levels of sputum TNFα and IL1β. γProteobacteria:Firmicutes (γP:F) differentiated the clusters and was the most predictive biomarker of the Haemophilus‐high group.

<![CDATA[Subphenotypes of nonsteroidal antiinflammatory disease‐exacerbated respiratory disease identified by latent class analysis]]> Heterogeneity of NERD phenotype reflects differences in inflammatory response measured by airway cells and eicosanoids. Identifying subphenotypes provides a more insightful perception and suggests a need for more individualized approach. In aspect of logLTE4/logPGE2 ratio, latent class analysis assigned subject to different groups better than identification by disease severity or control emphasizing the heterogeneity in NERD subgroup. Abbreviations: LTE4, Leukotriene E4; NERD, NSAID‐exacerbated respiratory disease; PGE2, Prostaglandin E2

<![CDATA[Eosinophils capture viruses, a capacity that is defective in asthma]]>



Activated eosinophils cause major pathology in stable and exacerbating asthma; however, they can also display protective properties like an extracellular antiviral activity. Initial murine studies led us to further explore a potential intracellular antiviral activity by eosinophils.


To follow eosinophil‐virus interaction, respiratory syncytial virus (RSV) and influenza virus were labeled with a fluorescent lipophilic dye (DiD). Interactions with eosinophils were visualized by confocal microscopy, electron microscopy, and flow cytometry. Eosinophil activation was assessed by both flow cytometry and ELISA. In a separate study, eosinophils were depleted in asthma patients using anti‐IL‐5 (mepolizumab), followed by a challenge with rhinovirus‐16 (RV16).


DiD‐RSV and DiD‐influenza rapidly adhered to human eosinophils and were internalized and inactivated (95% in ≤ 2 hours) as reflected by a reduced replication in epithelial cells. The capacity of eosinophils to capture virus was reduced up to 75% with increasing severity of asthma. Eosinophils were activated by virus in vitro and in vivo. In vivo this correlated with virus‐induced loss of asthma control.


This previously unrecognized and in asthma attenuated antiviral property provides a new perspective to eosinophils in asthma. This is indicative of an imbalance between protective and cytotoxic properties by eosinophils that may underlie asthma exacerbations.