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首页> 外文期刊>Infection and immunity >Expression and Bactericidal Activity of Nitric Oxide Synthase in Brucella suis-Infected Murine Macrophages
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Expression and Bactericidal Activity of Nitric Oxide Synthase in Brucella suis-Infected Murine Macrophages

机译：一氧化氮合酶在猪布鲁氏菌感染的小鼠巨噬细胞中的表达及杀菌活性

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We examined the expression and activity of inducible nitric oxide synthase (iNOS) in both gamma interferon (IFN-γ)-treated and untreated murine macrophages infected with the gram-negative bacteriumBrucella suis. The bacteria were opsonized with a mouse serum containing specific antibrucella antibodies (ops-Brucella) or with a control nonimmune serum (c-Brucella). The involvement of the produced NO in the killing of intracellular B. suis was evaluated. B. suis survived and replicated within J774A.1 cells. Opsonization with specific antibodies increased the number of phagocytized bacteria but lowered their intramacrophage development. IFN-γ enhanced the antibrucella activity of phagocytes, with this effect being greater inops-Brucella infection. Expression of iNOS, interleukin-6, and tumor necrosis factor alpha (TNF-α) mRNAs was induced in bothc-Brucella- and ops-Brucella-infected cells and was strongly potentiated by IFN-γ. In contrast to that of cytokine mRNAs, iNOS mRNA expression was independent of opsonization. Similar levels of iNOS mRNAs were expressed in IFN-γ-treated cells infected with c-Brucella or ops-Brucella; however, expression of iNOS protein and production of NO were detected only in IFN-γ-treated cells infected with ops-Brucella. These discrepencies between iNOS mRNA and protein levels were not due to differences in TNF-α production. The iNOS inhibitorNω-nitro-l-arginine methyl ester increasedB. suis multiplication specifically in IFN-γ-treated cells infected with ops-Brucella, demonstrating a microbicidal effect of the NO produced. This observation was in agreement with in vitro experiments showing that B. suiswas sensitive to NO killing. Together our data indicate that inB. suis-infected murine macrophages, the posttranscriptional regulation of iNOS necessitates an additive signal triggered by macrophage Fcγ receptors. They also support the possibility that in mice, NO favors the elimination ofBrucella, providing that IFN-γ and antibrucella antibodies are present, i.e., following expression of acquired immunity.
机译：我们检查了被革兰氏阴性细菌 Brucella suis 感染的γ干扰素（IFN-γ）处理和未处理的鼠巨噬细胞中诱导型一氧化氮合酶（iNOS）的表达和活性。用含有特异性抗小球藻抗体的小鼠血清（ ops-Brucella ）或对照非免疫血清（ c-Brucella ）对细菌进行调理。产生的NO参与细胞内 B的杀伤。 suis 进行了评估。 B。 suis 在J774A.1细胞中存活并复制。使用特异性抗体进行调理作用可增加吞噬细菌的数量，但会降低其巨噬细胞内的发育。 IFN-γ增强了吞噬细胞的抗小球藻活性，在 ops-Brucella 感染中这种作用更大。在感染了 c-Brucella -和 ops-Brucella 的细胞中均诱导了iNOS，白介素6和肿瘤坏死因子α（TNF-α）mRNA的表达。被IFN-γ强烈增强。与细胞因子mRNA相反，iNOS mRNA的表达与调理作用无关。在感染了 c-Brucella 或 ops-Brucella 的IFN-γ处理的细胞中，iNOS mRNA的表达水平相似。然而，仅在被 ops-Brucella 感染的IFN-γ处理的细胞中检测到iNOS蛋白的表达和NO的产生。 iNOS mRNA和蛋白质水平之间的这些差异并不是由于TNF-α产生的差异。 iNOS抑制剂 N ω-硝基-1-精氨酸甲酯增加了 B。 suis 专门在受 ops-Brucella 感染的IFN-γ处理的细胞中繁殖，证明产生的NO具有杀菌作用。该观察结果与显示 B的体外实验一致。 suis 对NO的杀死很敏感。我们的数据一起表明在 B中。被猪感染的鼠巨噬细胞，iNOS的转录后调控需要由巨噬细胞Fcγ受体触发的加性信号。他们还支持在小鼠中NO有助于消除 Brucella 的可能性，前提是存在IFN-γ和抗brucella抗体，即在表达获得性免疫后。

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