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首页> 外文期刊>Infection and immunity >Live Brucella spp. fail to induce tumor necrosis factor alpha excretion upon infection of U937-derived phagocytes.
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Live Brucella spp. fail to induce tumor necrosis factor alpha excretion upon infection of U937-derived phagocytes.

机译：活布鲁氏菌属。感染U937吞噬细胞后无法诱导肿瘤坏死因子α排泄。

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Tumor necrosis factor alpha (TNF-alpha) plays a central role in activation of first-line defenses of a host against foreign organisms. To determine whether Brucella infection modulated TNF-alpha production, we measured the biological activity of this cytokine in supernatants of U937 cell-derived macrophages and of fresh human monocytes infected with Brucella spp. Neither the smooth nor rough Brucella strains used induced any measurable TNF-alpha excretion upon infection. On the contrary, as reported before for other gram-negative bacteria, phagocytosis of nonpathogenic Escherichia coli was followed by a rapid and transient induction of TNF-alpha release, suggesting an involvement of this cytokine in some autocrine process. As expected, the Brucella strains tested survived and/or multiplied within U937-derived macrophages, whereas E. coli was rapidly eliminated after phagocytosis. Immunoglobulin G opsonization of E. coli strains enhanced their intracellular killing and strongly potentiated TNF-alpha secretion. Immunoglobulin G opsonization of Brucella strains, in contrast, did not lead to TNF-alpha production, although their rate of intracellular multiplication was reduced. Killed brucellae, however, promoted a significant excretion of TNF-alpha from U937-derived macrophages into cell culture supernatants. We finally demonstrated that pretreatment of U937-derived macrophages with exogenous TNF-alpha significantly inhibited intracellular multiplication of Brucella spp. These results and experiments performed on fresh human monocytes or with isolated lipopolysaccharide (LPS) showed that (i) differences in TNF-alpha production observed during macrophage infection by Brucella spp. and E. coli were not due to differences in LPS structure but resulted from active inhibition of TNF-alpha production by a specific process linked to Brucella spp. and (ii) the capacity of Brucella spp. to use pathways avoiding TNF-alpha production during infection may be considered a major attribute of virulence.
机译：肿瘤坏死因子α（TNF-alpha）在激活宿主对抗外来生物的一线防御中起着核心作用。为了确定布鲁氏菌感染是否调节了TNF-α的产生，我们测量了U937细胞衍生的巨噬细胞和感染布鲁氏菌属物种的新鲜人类单核细胞上清液中该细胞因子的生物活性。使用的光滑或粗糙布鲁氏菌菌株均不会在感染后诱导任何可测量的TNF-α排泄。相反，如先前针对其他革兰氏阴性细菌的报道，在非致病性大肠杆菌的吞噬作用之后，迅速而短暂地诱导了TNF-α的释放，表明该细胞因子参与了某些自分泌过程。正如预期的那样，测试的布鲁氏菌菌株在U937衍生的巨噬细胞中存活和/或繁殖，而大肠杆菌在吞噬作用后迅速被消除。大肠杆菌菌株的免疫球蛋白G调理作用可增强其细胞内杀伤力并增强TNF-α的分泌。相比之下，布鲁氏菌菌株的免疫球蛋白G调理作用虽然导致细胞内增殖的速率降低，但并未导致TNF-α的产生。但是，杀死的布鲁氏菌会促使TNF-α从U937衍生的巨噬细胞中大量排泄到细胞培养上清液中。我们最终证明，用外源性TNF-α预处理U937衍生的巨噬细胞可显着抑制布鲁氏菌属细胞的细胞内增殖。这些结果和对新鲜人单核细胞或分离的脂多糖（LPS）进行的实验表明，（i）在布鲁氏菌属巨噬细胞感染过程中观察到的TNF-α产生差异。大肠杆菌和大肠杆菌不是由于LPS结构的差异，而是由于与布鲁氏菌属有关的特定过程对TNF-α产生的主动抑制所致。 （ii）布鲁氏菌属的能力。使用途径来避免感染期间TNF-α的产生可能被认为是毒力的主要属性。

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