NITRIC-OXIDE MEDIATES INTESTINAL PATHOLOGY IN GRAFT-VS-HOST DISEASE
NITRIC-OXIDE MEDIATES INTESTINAL PATHOLOGY IN GRAFT-VS-HOST DISEASE
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DOI：
10.1002/eji.1830220827
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发表时间：
1992-08-01
影响因子：
5.4
通讯作者：
MOWAT, AM
中科院分区：
文献类型：
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作者：
GARSIDE, P;HUTTON, AK;MOWAT, AM
我们研究了一氧化氮（NO）在小鼠肠道移植物抗宿主反应（GvHR）中的作用。用NO合成的特异性抑制剂L-N（G）-单甲基精氨酸（L-NMMA）处理小鼠，消除了肠GvHR的粘膜病理学，并减少了相关的上皮淋巴细胞浸润。L-NMMA对GvHR中的脾肿大没有影响，也不干扰未分化的隐窝干细胞系的生长，或体外活化的巨噬细胞产生肿瘤坏死因子-α。相反，L-NMMA抑制了GvHR中发生的自然杀伤（NK）细胞的增强活性。我们的结论是一个NO依赖的机制是必不可少的肠道免疫病理学GvHR，这可能反映了一个作用，在NK细胞功能的NO。
We have investigated the involvement of nitric oxide (NO) in intestinal graft-vs. -host reaction (GvHR) in mice. Treatment of mice with L-N(G)-monomethyl arginine (L-NMMA), a specific inhibitor of NO synthesis, abolished the mucosal pathology of intestinal GvHR and reduced the associated lymphocytic infiltration of the epitheliUM. L-NMMA had no effect on splenomegaly in GvHR, nor did it interfere with the growth of an undifferentiated crypt stem cell line, or the production of tumor necrosis factor-alpha by activated macrophages in vitro. In contrast, L-NMMA inhibited the enhanced activity of natural killer (NK) cells which occurs in GvHR. We conclude that a NO-dependent mechanism is essential for intestinal immunopathology in GvHR and that this may reflect a role for NO in NK cell function.