Deletion of Regulatory T cells supports the development of intestinal ischemia/reperfusion injuries

• 作 者: Xuekang Yang Dahai Hu Hua Bai Yunchuan Wang Jun Li Qin Zhou Weixia Cai Juntao Han Xiongxiang Zhu Maolong Dong
• 机 构: Department of Burns and Cutaneous Surgery,Xijing Hospital,The Fourth Military Medical University,Xi
• 出 处: 2013年全军烧伤外科学术年会
• 发表日期: 2013年12期
• 关键词: Regulatory T cells Small intestine Ischemia reperfusion Inflammation.

　　Background: Ischemia/reperfusion injury (IRI) of the intestine is associated with a high morbidity and mortality in surgical and trauma patients.T cells participate in the pathogenesis of intestinal IRI, and T cell depletion has been shown to inhibit inflammatory responses and diminish intestinal damage.However, the mechanism by which T cells contribute to intestinal IRI is not completely understood.Regulatory T cells (Tregs) are a specific subset of T cells that suppress immune responses and protect against tissue injuries.We hypothesized that Tregs might be involved in intestinal IRI.Materials and methods: C57/B16 mice were subjected to 30 minutes of ischemia by clamping the superior mesenteric artery followed by reperfusion.Animals were pretreated with the anti-CD25 monoclonal antibody or adoptive transfer of Tregs before induction of IRI.The number of inflammatory cells, the level of inflammatory factors and intestinal permeability was assessed,Results: Partial depletion of Tregs with an anti-CD25 monoclonal antibody potentiated intestinal permeability induced by IRI.The Treg-depleted mice showed more neutrophils and CD4+ T cells.In addition, depletion of Tregs led to enhanced secretion of tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), and interleukin (IL)-4 and reduced levels of IL-10.Furthermore, we performed adoptive transfer of Tregs and found that transfer of Tregs significantly inhibited the ischemia/reperfusion-induced increase of intestinal permeability.Conclusions: Our study indicated that Tregs participate in intestinal inflammatory responses induced by IRI and that targeting Tregs could be a novel therapeutic approach to intestinal IRI.