Salmonella typhimurium infection in mice induces nitric oxide-mediated immunosuppression through a natural killer cell-dependent pathway.
Salmonella typhimurium infection in mice induces nitric oxide-mediated immunosuppression through a natural killer cell-dependent pathway.
复制标题
小鼠鼠伤寒沙门氏菌感染通过自然杀伤细胞依赖性途径诱导一氧化氮介导的免疫抑制。
DOI：
10.1128/iai.66.12.5862-5866.1998
复制
发表时间：
1998
影响因子：
3.1
通讯作者：
Eisenstein,TK
中科院分区：
文献类型：
--
作者：
Schwacha,MG;MeisslerJr,JJ;Eisenstein,TK
接种鼠伤寒沙门氏菌减毒株3至7天后，从C57BL/6J雌性小鼠中分离出的脾细胞产生高水平的一氧化氮（39至77μM）和γ干扰素（IFN-γ）。此外，接种沙门氏菌的小鼠的脾细胞培养物对绵羊红细胞产生体外空斑形成细胞（PFC）反应的能力明显受到抑制。免疫脾细胞群中自然杀伤 (NK) 细胞的耗竭显着减少了一氧化氮的产生，防止了 PFC 反应的抑制，并完全消除了 IFN-γ 的释放。用 IFN-γ 处理 NK 细胞耗尽的免疫细胞，可以将一氧化氮的产生恢复到与完整免疫细胞相当的水平，并恢复免疫抑制。这些结果表明，NK 细胞在感染链球菌后调节一氧化氮介导的免疫抑制的诱导。鼠伤寒杆菌通过产生 IFN-γ。
Splenocytes isolated from C57BL/6J female mice 3 to 7 days after inoculation with an attenuated strain ofSalmonella typhimuriumproduced high levels of nitric oxide (39 to 77 μM) and gamma interferon (IFN-γ). Additionally, spleen cell cultures fromSalmonella-inoculated mice were markedly suppressed in their ability to generate an in vitro plaque-forming cell (PFC) response to sheep erythrocytes. Depletion of natural killer (NK) cells from the immune splenocyte population markedly reduced nitric oxide production, prevented suppression of PFC responses, and completely abrogated IFN-γ release. Treatment of NK cell-depleted immune cells with IFN-γ restored nitric oxide production to levels comparable to those of intact immune cells and also restored the immunosuppression. These results suggest that NK cells regulate the induction of nitric oxide-mediated immunosuppression following infection withS. typhimuriumthrough the production of IFN-γ.