Bystander injury of host lymphoid tissue during murine graft-verus-host disease is mediated by nitric oxide.
Bystander injury of host lymphoid tissue during murine graft-verus-host disease is mediated by nitric oxide.
复制标题
小鼠移植物抗宿主病期间宿主淋巴组织的旁观者损伤是由一氧化氮介导的。
DOI：
10.1097/00007890-199602270-00016
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发表时间：
1996
期刊：
影响因子：
6.2
通讯作者：
Simmons,RL
中科院分区：
文献类型：
--
作者：
Hoffman,RA;Langrehr,JM;Berry,LM;White,DA;Schattenfroh,NC;McCarthy,SA;Simmons,RL
移植物抗宿主病（GVHD）特征性的淋巴细胞增殖反应受到抑制，部分原因是一氧化氮（NO）的产生。为进一步阐明NO在GVHD中的作用，用NO合成抑制剂氨基胍（AG）对未照射的（C57 BL/6 J × DBA/2 J）F1小鼠注射5× 107个C57 BL/6 J脾细胞。应用AG可使GVHD时血清NO2-+ NO3-水平升高消失.宿主表型（H2 B/d、B220+和THY 1）的脾细胞百分比显著增加。在接受AG治疗的GVHD动物中检测到显著更高的血细胞比容值。此外，从接受AG治疗的GVHD小鼠中获得的脾细胞的Con A诱导的增殖反应与未接受AG治疗的动物的脾细胞的反应相比增加。不受AG治疗影响的参数包括恢复的腹腔巨噬细胞的NO合成、脾细胞群中的供体抗宿主细胞溶解活性、血清GM-CSF水平和供体细胞的长期植入。这些数据表明，NO可能在淋巴和红系宿主组织的破坏以及与GVHD急性期相关的淋巴细胞增殖反应降低中发挥作用。
The suppressed lymphocyte proliferative responses characteristic of graft-versus-host disease (GVHD) are due, in part, to production of nitric oxide (NO). In order to more fully elucidate the role of NO during GVHD, an NO synthesis inhibitor, aminoguanidine (AG), was administered to unirradiated (C57BL/6J× DBA/2J) F 1 mice injected with 5× 10 7 C57BL/6J splenocytes. Administration of AG resulted in abrogation of the elevation in serum NO 2-+ NO 3-levels characteristic of GVHD. A significantly increased percentage of splenocytes of host phenotype (H2 b/d, B220+, and THY1. 2+) and a significantly higher hematocrit value were detected in GVHD animals receiving AG therapy. Additionally, the Con A-induced proliferative response of splenocytes obtained from GVHD mice receiving AG therapy was increased compared with the responses of splenocytes from animals that did not receive AG therapy. Parameters not affected by AG therapy included NO synthesis by recovered peritoneal macrophages, donor antihost cytolytic activity in splenocyte populations, serum GM-CSF levels and long-term engraftment of donor cells. These data indicate that NO may play a role in the destruction of both lymphoid and erythroid host tissue as well as the reduced lymphoproliferative responses associated with the acute phase of GVHD.