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首页> 外文期刊>Infection and immunity >In Vivo Blockage of Nitric Oxide with Aminoguanidine Inhibits Immunosuppression Induced by an Attenuated Strain of Salmonella typhimurium, PotentiatesSalmonella Infection, and Inhibits Macrophage and Polymorphonuclear Leukocyte Influx into the Spleen
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In Vivo Blockage of Nitric Oxide with Aminoguanidine Inhibits Immunosuppression Induced by an Attenuated Strain of Salmonella typhimurium, PotentiatesSalmonella Infection, and Inhibits Macrophage and Polymorphonuclear Leukocyte Influx into the Spleen

机译：一氧化氮与氨基胍的体内阻断抑制了鼠伤寒沙门氏菌减毒株诱导的免疫抑制，增强了沙门氏菌感染，并抑制了巨噬细胞和多形核白细胞向脾脏的流入。

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Our laboratory has previously shown that after immunization with a strain of Salmonella typhimurium, SL3235, made avirulent by a blockage in the pathway of aromatic synthesis, murine splenocytes were profoundly suppressed in their capacity to mount an in vitro antibody plaque-forming cell (PFC) response to sheep erythrocytes. Evidence indicated that suppression was mediated by nitric oxide (NO), since the in vitro addition ofN G-monomethyl-l-arginine blocked suppression. The present studies examined the effect of blocking NO production on Salmonella-induced immunosuppression by in vivo administration of aminoguanidine hemisulfate (AG). AG was administered to C3HeB/FeJ mice in their drinking water (2.5% solution) for 7 days prior to intraperitoneal inoculation with SL3235. AG treatment inhibited the increase in nitrate and nitrite levels in plasma and nitrite levels in the spleen seen in immunized mice. Importantly, AG treatment completely blocked suppression of the splenic PFC response and markedly attenuated the suppression of the response to concanavalin A in immunized mice, providing further evidence thatSalmonella-induced immunosuppression is mediated by NO. AG treatment also alleviated the majority of the splenomegaly associated with SL3235 inoculation, which correlated with a blockage of influx of neutrophils and macrophages into spleens, as assessed by flow cytometry. AG treatment unexpectedly resulted in 90% mortality in mice injected with the highly attenuated vaccine strain ofSalmonella, SL3235. Increased mortality in AG-treated mice correlated with inability to clear organisms from the spleen by day 15 postinoculation and with persistent bacteremia, compared with control mice. Collectively, these in vivo results underscore the dual biological consequences of NO production followingSalmonella infection, with NO being necessary for host defense, but also having the potentially adverse effect of immunosuppression. A unifying hypothesis to explain how these seemingly paradoxical effects could both result from NO production is presented.
机译：我们的实验室以前表明，用芳香族合成途径受阻的鼠伤寒沙门氏菌菌株SL3235免疫后，鼠脾细胞的体外抗体安装能力受到了显着抑制。斑块形成细胞（PFC）对绵羊红细胞的反应。有证据表明抑制作用是由一氧化氮（NO）介导的，因为在体外添加 N G -单甲基-1-精氨酸会抑制抑制作用。本研究通过体内施用氨基胍半硫酸盐（AG）检验了阻断NO产生对沙门氏菌诱导的免疫抑制的作用。在腹膜内接种SL3235之前，将AG的饮用水（2.5％溶液）给药于C3HeB / FeJ小鼠7天。 AG处理抑制了免疫小鼠中血浆中硝酸盐和亚硝酸盐水平的增加以及脾脏中亚硝酸盐水平的增加。重要的是，AG处理完全阻断了免疫小鼠的脾脏PFC应答抑制作用，并显着减弱了对伴刀豆球蛋白A应答的抑制作用，这进一步证明了沙门氏菌诱导的免疫抑制是由NO介导的。通过流式细胞术评估，AG治疗还减轻了与SL3235接种相关的大部分脾肿大，这与嗜中性粒细胞和巨噬细胞流入脾脏的阻塞有关。 AG治疗出乎意料地导致了注射高度减毒的沙门氏菌SL3235疫苗株的小鼠死亡率达到90％。与对照小鼠相比，经AG治疗的小鼠死亡率增加与接种后第15天无法从脾脏清除微生物以及持续的菌血症有关。总的来说，这些体内结果强调了沙门氏菌感染后NO产生的双重生物学后果，NO对于宿主防御是必需的，但也具有免疫抑制的潜在不利作用。提出了一个统一的假设来解释这些看似矛盾的效应如何同时由NO产生而产生。

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