Bryson J Scott, Brandon J Anthony, Jennings C Darrell, Kaplan Alan M
Division of Hematology and Blood & Marrow Transplantation, Department of Internal Medicine; University of Kentucky Medical Center, University of Kentucky, Lexington, KY USA.
Chimerism. 2011 Apr;2(2):58-60. doi: 10.4161/chim.2.2.16783.
Murine syngeneic graft-versus-host disease (SGVHD) results in chronic colon and liver inflammation following syngeneic bone marrow transplantation (BMT) and treatment with the calcineurin inhibitor, cyclosporine A (CsA). SGVHD was initially thought to arise as a result of an autoreactive immune response, but more recently it has been shown that enhanced antimicrobial responses develop in SGVHD mice. Consequently, we performed studies to analyze the role of the microbiota in the development of murine SGVHD. Treatment with broad-spectrum antibiotics eliminated disease-associated inflammatory immune responses and pathology, linking the role of the microbiota and microbial-specific immunity to the development of murine SGVHD. In a broader context, these results bring into question the role that anti-microbial immune responses play in post-transplant immune pathologies that develop following allogeneic stem cell transplantation and use of calcineurin inhibitors.
小鼠同基因移植物抗宿主病（SGVHD）在同基因骨髓移植（BMT）并用钙调神经磷酸酶抑制剂环孢素A（CsA）治疗后会导致慢性结肠和肝脏炎症。SGVHD最初被认为是自身反应性免疫反应的结果，但最近研究表明，SGVHD小鼠中会出现增强的抗菌反应。因此，我们开展了研究以分析微生物群在小鼠SGVHD发生过程中的作用。用广谱抗生素治疗消除了与疾病相关的炎症免疫反应和病理变化，将微生物群和微生物特异性免疫的作用与小鼠SGVHD的发生联系起来。从更广泛的背景来看，这些结果使人质疑抗菌免疫反应在异基因干细胞移植和使用钙调神经磷酸酶抑制剂后发生的移植后免疫病理中所起的作用。
