ArticleFrontiers in cellular and infection microbiology2025
Influenza-induced microRNA-155 expression is altered in extracellular vesicles derived from the COPD epithelium.
Article in Frontiers in cellular and infection microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Influenza virus particularly affects those with chronic lung conditions such as Chronic Obstructive Pulmonary Disease (COPD). Airway epithelial cells are the first line of defense and primary target of influenza infection and release extracellular vesicles (EVs). EVs can transfer of biological molecules such as microRNAs (miRNAs) that can modulate the immune response to viruses through control of the innate and adaptive immune systems. The aim of this work was to profile the EV miRNAs released from bronchial epithelial cells in response to influenza infection and discover if EV miRNA expression was altered in COPD. Methods: Influenza infection of air-liquid interface (ALI) differentiated BCi-NS1.1 epithelial cells were characterized by analyzing the expression of antiviral genes, cell barrier permeability and cell death. EVs were isolated by filtration and size exclusion chromatography from the apical surface wash of ALI cultured bronchial epithelial cells. The EV miRNA cargo was sequenced and reads mapped to miRBase. The BCi sequencing results were further investigated by RT-qPCR and by using healthy and COPD primary epithelial cells. Results: Infection of ALI cultured BCi cells with IAV at 3.6 x 10 Conclusion: Epithelial EV miRNA release may be a key mechanism in modulating the response to IAV in the lungs. Furthermore, changes in EV miRNA expression may play a dysfunctional role in influenza-induced exacerbations of COPD. However, further work to fully characterize the function of EV miRNA in response to IAV in both health and COPD is required.
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