Mucosal Inflammation Program, School of Medicine, University of Colorado – Anschutz Medical Campus, Aurora, Colorado, USA. Institute of Immunology, Department of Biology, Maynooth University, County Kildare, Ireland.
Address correspondence to: Eóin N. McNamee, Institute of Immunology, Department of Biology, Maynooth University, County Kildare, Ireland. Phone: 353.1.708.6369; Email: firstname.lastname@example.org.
First published January 14, 2019 - More info
A predominant feature of intestinal inflammation is the accumulation of neutrophils, which dictates a fine balance between epithelial repair or progression to chronic inflammation. While the processes of mucosal healing are well studied, how neutrophils advance an inflammatory insult towards epithelial neoplasia is less understood. In this issue of the JCI, Butin-Israeli et al. outline a mechanism whereby neutrophils control epithelial fitness and genomic instability via delivery of miR-23a–and miR-155–containing microparticles. Localized delivery of antisense oligonucleotides targeting miR-23a and miR-155 reversed this genomic instability and accelerated mucosal healing. This mechanism of neutrophil-derived microRNA shuttling opens up new therapeutic potential to enhance epithelial healing and limit mucosal injury.
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