Fuji Shigeo, Kapp Markus, Einsele Hermann
Division of Hematology, Department of Internal Medicine II, University Hospital of Würzburg , Würzburg , Germany ; Division of Hematopoietic Stem Cell Transplantation, National Cancer Center Hospital , Tokyo , Japan.
Division of Hematology, Department of Internal Medicine II, University Hospital of Würzburg , Würzburg , Germany.
Front Oncol. 2014 Apr 24;4:89. doi: 10.3389/fonc.2014.00089. eCollection 2014.
Graft-versus-host disease (GVHD) is still one of the major causes of morbidity and mortality in allogeneic hematopoietic stem cell transplantation (HSCT). In the pathogenesis of acute GVHD, it has been established that donor-derived T-cells activated in the recipient play a major role in GVHD in initiation and maintenance within an inflammatory cascade. To reduce the risk of GVHD, intensification of GVHD prophylaxis like T-cell depletion is effective, but it inevitably increases the risk of infectious diseases and abrogates beneficial graft-versus-leukemia effects. Although various cytokines are considered to play an important role in the pathogenesis of GVHD, GVHD initiation is such a complex process that cannot be prevented by means of single inflammatory cytokine inhibition. Thus, efficient methods to control the whole inflammatory milieu both on cellular and humoral view are needed. In this context, infectious diseases can theoretically contribute to an elevation of inflammatory cytokines after allogeneic HSCT and activation of various subtypes of immune effector cells, which might in summary lead to an aggravation of acute GVHD. The appropriate treatments or prophylaxis of bacterial infection during the early phase after allogeneic HSCT might be beneficial to reduce not only infectious-related but also GVHD-related mortality. Here, we aim to review the literature addressing the interactions of bacterial infections and GVHD after allogeneic HSCT.
移植物抗宿主病（GVHD）仍然是异基因造血干细胞移植（HSCT）中发病和死亡的主要原因之一。在急性移植物抗宿主病的发病机制中，已证实受体中被激活的供体来源T细胞在炎症级联反应的起始和维持阶段的移植物抗宿主病中起主要作用。为降低移植物抗宿主病的风险，强化移植物抗宿主病预防措施（如T细胞清除）是有效的，但这不可避免地增加了感染性疾病的风险，并消除了有益的移植物抗白血病效应。尽管各种细胞因子被认为在移植物抗宿主病的发病机制中起重要作用，但移植物抗宿主病的起始是一个如此复杂的过程，无法通过单一炎症细胞因子抑制来预防。因此，需要从细胞和体液角度控制整个炎症环境的有效方法。在这种情况下，理论上感染性疾病可导致异基因造血干细胞移植后炎症细胞因子升高和各种免疫效应细胞亚型激活，这可能总体上导致急性移植物抗宿主病加重。异基因造血干细胞移植后早期对细菌感染进行适当治疗或预防可能不仅有利于降低感染相关死亡率，也有利于降低移植物抗宿主病相关死亡率。在此，我们旨在综述关于异基因造血干细胞移植后细菌感染与移植物抗宿主病相互作用的文献。
