论文作者、美国维克森林大学浸礼会医学中心再生医学研究所( Wake Forest University Baptist Medical Center's Institute for Regenerative Medicine)教授Graca Almeida-Porada博士说，"这些干细胞参与血管形成，而且证实它可能能够被用来改善在炎症性肠病病人体内发现的血管异常。" 炎症性肠病的两个特征就是经常性腹泻和腹痛。它实际上就相当于两种疾病---溃疡性结肠炎(ulcerative colitis)和克罗恩氏病(Crohn's disease)。在炎症性肠病中，肠道变得红肿，并患上溃疡，同时肠道中的血管泄漏而导致炎症产生。在这项研究中，还研究了一种特殊的内皮集落形成细胞(endothelial colony-formingcell)群体。这些细胞是在脐带血、骨髓和循环血液中发现的，能够不仅在胚胎中而且也能在成人体内促进血管形成。对人的研究已证实这些细胞能够改善四肢中的血流量减少，因而还能够用于心脏病治疗。

    炎症性肠病又称肠炎，是一组肠道炎症性疾病的统称。一般指大肠内的炎症，有时候也被用来指小肠内的炎症。虽然目前还没有治疗炎症性肠病的手段，但有药物可以治疗减轻炎症和防止免疫反应。然而，这些疗法并不总是有效的。研究人员的目标就是开发一种可注射的细胞疗法，促使小肠组织恢复，目前实验已经证明脐带血中的干细胞能够迁移到健康肠道，并在那里存活下来，同时也有潜力维持血管健康。

    脐带血干细胞疗法，在未来有望发展成为有效治疗炎症性肠病的新趋势。

    推荐原文阅读：

    Hepatology. 2012 Sep;56(3):1086-96.

    Distinct contribution of human cord blood-derived endothelial colony forming cells to liver and gut in a fetal sheepmodel.

    Wood JA, Colletti E, Mead LE, Ingram D,Porada CD, Zanjani ED, Yoder MC, Almeida-Porada G.

    Source

    Department of Animal Biotechnology, University of Nevada, Reno, NV, USA.

    Abstract

    Although the vasculogenic potential of circulating and cord blood (CB)-derived endothelial colony-forming cells (ECFC) has been demonstrated in vitro and in vivo, little is known about the inherent biologic ability of these cells to home to different organs and contribute to tissue-specific cell populations. Here we used a fetal sheep model of in utero transplantation to investigate and compare the intrinsic ability of human CB-derived ECFC to migrate to the liver and to the intestine, and to define ECFC's intrinsic ability to integrate and contribute to the cytoarchitecture of these same organs. ECFCs were transplanted by an intraperitoneal or intrahepatic route (IH) into fetal sheep at concentrations ranging from 1.1-2.6 × 10(6)cells/fetus. Recipients were evaluated at 85 days posttransplant for donor (human) cells using flow cytometry and confocal microscopy. We found that, regardless of the route of injection, and despite the IH delivery of ECFC, the overall liver engraftment was low, but a significant percentage ofcells were located in the perivascular regions and retained the expression of hallmark endothelial makers. By contrast, ECFC migrated preferentially to the intestinal crypt region and contributed significantly to the myofibroblast population. Furthermore, ECFC expressing CD133 and CD117 lodged in areas where endogenous cells expressed those same phenotypes.

    CONCLUSION:

    ECFC inherently constitute a potential source of cells for the treatment of intestinal diseases, but strategies to increase the numbers of ECFC persisting within the hepatic parenchyma are needed in order to enhance ECFC therapeutic potential for this organ.