Communication between myeloid cells and epithelium plays critical role in maintaining intestinal epithelial barrier integrity. Myeloid cells interact with intestinal epithelial cells (IEC s) by producing various mediators; however, the molecules mediating their crosstalk remain incompletely understood. Here, we report that deficiency of angiogenin (Ang ) in mouse myeloid cells caused impairment of epithelial barrier integrity, leading to high susceptibility to DSS ‐induced colitis. Mechanistically, myeloid cell‐derived angiogenin promoted IEC survival and proliferation through plexin‐B2‐mediated production of tRNA ‐derived stress‐induced small RNA (tiRNA ) and transcription of ribosomal RNA (rRNA ), respectively. Moreover, treatment with recombinant angiogenin significantly attenuated the severity of experimental colitis. In human samples, the expression of angiogenin was significantly down‐regulated in patients with inflammatory bowel disease (IBD ). Collectively, we identified, for the first time to our knowledge, a novel mediator of myeloid cell‐IEC crosstalk in maintaining epithelial barrier integrity, suggesting that angiogenin may serve as a new preventive agent and therapeutic target for IBD.

中文翻译：

---

髓样细胞通过血管生成素/ plexin-B2轴保护肠道上皮屏障的完整性。

髓样细胞与上皮细胞之间的通讯在维持肠上皮屏障完整性方面起着至关重要的作用。髓样细胞通过产生各种介体与肠道上皮细胞（IEC s）相互作用。然而，介导其串扰的分子仍未完全了解。在这里，我们报告说血管生成素缺乏症（Ang）在小鼠骨髓细胞中导致上皮屏障完整性受损，导致对DSS诱发的结肠炎的高度敏感性。从机制上讲，髓细胞源性血管生成素分别通过plexin-B2介导的tRNA产生的应激诱导小RNA（tiRNA）和核糖体RNA（rRNA）的转录来促进IEC存活和增殖。而且，用重组血管生成素治疗显着减轻了实验性结肠炎的严重性。在人类样品中，炎症性肠病（IBD）患者的血管生成素表达显着下调。总体而言，我们首次了解到，在维持上皮屏障完整性方面，一种新的髓样细胞-IEC串扰介导的介质，