Song Eun Mi, Jung Sung Ae, Lee Ko Eun, Jang Ji Young, Lee Kang Hoon, Tae Chung Hyun, Moon Chang Mo, Joo Yang Hee, Kim Seong Eun, Jung Hye Kyung, Shim Ki Nam
Department of Internal Medicine, Ewha Medical Research Institute, Ewha Womans University School of Medicine, Seoul, Korea.
Korean J Gastroenterol. 2017 Feb 25;69(2):119-128. doi: 10.4166/kjg.2017.69.2.119.
BACKGROUND/AIMS: Mesenchymal stem cells (MSCs) are multipotent progenitor cells currently under investigation for its efficacy as the treatment for inflammatory bowel disease. In this study, we evaluated the efficacy of tonsil-derived mesenchymal stem cells (T-MSCs) as a novel source of mesenchymal stem cells and traced their localization in a murine model of acute colitis induced by dextran sulfate sodium (DSS).
C57BL/6 mice were randomly assigned to the following three groups: the normal control group, DSS colitis group (DSS+phosphate buffered saline), and T-MSC group (DSS+T-MSCs, 1×10). The severity of colitis was assessed by determining the severity of symptoms of colitis, colon length, histopathologic grade, and levels of inflammatory cytokines. T-MSCs labeled with PKH26 were traced .
The T-MSC group, compared with the DSS colitis group, showed a significantly lower disease activity index (11.3±1.5 vs. 8.3±1.9, p=0.015) at sacrifice and less reduction of body weight (-17.1±5.0% vs. -8.1±6.9%, p=0.049). In the T-MSC group, the histologic colitis score was significantly decreased compared with the DSS colitis group (22.6±3.8 vs. 17.0±3.4, p=0.039). IL-6 and IL-1β, the pro-inflammatory cytokines, were also significantly reduced after a treatment with T-MSCs. tracking revealed no PKH26-labelled T-MSCs in the colonic tissue of mice with acute colitis.
In the acute colitis model, we demonstrated that the administration of T-MSCs ameliorates inflammatory symptoms and histology. Moreover, the anti-inflammatory activities of T-MSCs were independent of gut homing.
背景/目的：间充质干细胞（MSCs）是多能祖细胞，目前正在研究其作为治疗炎症性肠病的疗效。在本研究中，我们评估了扁桃体来源的间充质干细胞（T-MSCs）作为间充质干细胞新来源的疗效，并在葡聚糖硫酸钠（DSS）诱导的急性结肠炎小鼠模型中追踪了它们的定位。
将C57BL/6小鼠随机分为以下三组：正常对照组、DSS结肠炎组（DSS+磷酸盐缓冲盐水）和T-MSC组（DSS+T-MSCs，1×10）。通过确定结肠炎症状的严重程度、结肠长度、组织病理学分级和炎性细胞因子水平来评估结肠炎的严重程度。追踪用PKH26标记的T-MSCs。
与DSS结肠炎组相比，T-MSC组在处死时疾病活动指数显著降低（11.3±1.5对8.3±1.9，p=0.015），体重减轻较少（-17.1±5.0%对-8.1±6.9%，p=0.049）。在T-MSC组中，组织学结肠炎评分与DSS结肠炎组相比显著降低（22.6±3.8对17.0±3.4，p=0.039）。用T-MSCs治疗后，促炎细胞因子IL-6和IL-1β也显著降低。追踪显示，急性结肠炎小鼠的结肠组织中没有PKH26标记的T-MSCs。
在急性结肠炎模型中，我们证明了T-MSCs的给药可改善炎症症状和组织学。此外，T-MSCs的抗炎活性与肠道归巢无关。
