J Clin Invest. 2019 Feb 1;129(2):499-502. doi: 10.1172/JCI125779. Epub 2019 Jan 14.
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.
肠道炎症的一个主要特征是中性粒细胞的积累，这决定了上皮修复或进展为慢性炎症之间的微妙平衡。虽然黏膜愈合过程已经得到很好的研究，但中性粒细胞如何将炎症损伤推进为上皮肿瘤仍知之甚少。在本期 JCI 中，Butin-Israeli 等人概述了一种机制，即中性粒细胞通过递送含有 miR-23a 和 miR-155 的微颗粒来控制上皮细胞的适应性和基因组不稳定性。针对 miR-23a 和 miR-155 的反义寡核苷酸的局部递送逆转了这种基因组不稳定性并加速了黏膜愈合。这种中性粒细胞衍生的 microRNA 转运的机制为增强上皮细胞愈合和限制黏膜损伤开辟了新的治疗潜力。
