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首页> 外文期刊>Infection and immunity >Role of inorganic nitrogen oxides and tumor necrosis factor alpha in killing Leishmania donovani amastigotes in gamma interferon-lipopolysaccharide-activated macrophages from Lshs and Lshr congenic mouse strains.
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Role of inorganic nitrogen oxides and tumor necrosis factor alpha in killing Leishmania donovani amastigotes in gamma interferon-lipopolysaccharide-activated macrophages from Lshs and Lshr congenic mouse strains.

机译：无机氮氧化物和肿瘤坏死因子α在杀死Lshs和Lshr同系小鼠品系的γ干扰素-脂多糖激活的巨噬细胞中杀灭利什曼原虫amastigotes的作用。

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The capacity of mature bone-marrow-derived macrophages and resident peritoneal macrophages from Lshr versus Lshs congenic mice to kill intracellular Leishmania donovani amastigotes when activated by recombinant gamma interferon-lipopolysaccharide (rIFN-gamma-LPS) was examined. IFN-gamma alone in doses up to 100 U/ml was unable to activate macrophages to kill L. donovani amastigotes in vitro; LPS was a necessary secondary stimulus. Similarly, LPS alone in doses up to 100 ng/ml produced no leishmanicidal activity. In bone marrow macrophages, a dose-dependent increase in leishmanicidal activity was observed as increasing rIFN-gamma-LPS dose combinations were introduced, with Lshr macrophages maintaining a significant but not dramatic advantage within any particular dose combination. For peritoneal macrophages, the reverse was true, with macrophages from Lshs mice being more efficient at killing for doses of LPS up to 10 ng/ml with doses of rIFN-gamma in the range of 11 to 33 U/ml. The degree of killing in both bone marrow and peritoneal macrophages correlated well with the levels of nitrites measured in the supernatants at 72 h, and a highly significant correlation was observed between 4-, 24-, or 72-h tumor necrosis factor alpha (TNF-alpha) release and nitrite production measured at 72 h. Inclusion of 200 microM NG-monomethyl-L-arginine, a competitive inhibitor of the L-arginine-dependent pathway for the synthesis of inorganic nitrogen oxides, inhibited the killing, as did the addition of neutralizing anti-TNF-alpha antibody. These results are consistent with previous data showing an important autocrine role for TNF-alpha in enhancing production of inorganic nitrogen oxides by primed or activated macrophages. In addition, our results suggest that production of TNF-alpha and nitrites after priming or activation signals may be under a different regulatory control in mature bone marrow macrophages than in the resident peritoneal macrophage population.
机译：检查了Lshr与Lshs同系小鼠的成熟骨髓衍生巨噬细胞和常驻腹膜巨噬细胞在被重组γ-干扰素-脂多糖（rIFN-γ-LPS）激活后杀死细胞内利什曼原虫amastigotes的能力。单独的剂量高达100 U / ml的IFN-γ无法激活巨噬细胞以杀死体外的L. donovani amastigotes。 LPS是必要的次级刺激。同样，单独的LPS最高剂量为100 ng / ml时也不会产生杀螨活性。在骨髓巨噬细胞中，随着引入的rIFN-γ-LPS剂量组合的增加，观察到了杀螨活性的剂量依赖性增加，而Lshr巨噬细胞在任何特定剂量组合中均保持了显着但非显着的优势。对于腹膜巨噬细胞，情况恰恰相反，来自Lshs小鼠的巨噬细胞在杀死rPS-γ剂量高达10 ng / ml且rIFN-γ剂量在11至33 U / ml的范围内时更有效地杀伤。骨髓和腹膜巨噬细胞的杀伤程度与72小时上清液中的亚硝酸盐水平密切相关，并且在4、24或72小时的肿瘤坏死因子α（TNF）之间观察到高度相关α-释放）和在72小时测量的亚硝酸盐生成。包括200 microM NG-单甲基-L-精氨酸，一种用于合成无机氮氧化物的L-精氨酸依赖性途径的竞争性抑制剂，与添加中和性抗TNF-α抗体一样，抑制了杀伤。这些结果与先前的数据相一致，先前的数据表明TNF-α在通过引发或活化的巨噬细胞增强无机氮氧化物的产生中具有重要的自分泌作用。此外，我们的研究结果表明，在成熟的骨髓巨噬细胞中，在引发或激活信号后，TNF-α和亚硝酸盐的产生可能处于与常驻腹膜巨噬细胞群体不同的调节控制之下。

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