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首页> 外文期刊>Infection and immunity >Resistance of Macrophages to Mycobacterium avium Is Induced by α2-Adrenergic Stimulation
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Resistance of Macrophages to Mycobacterium avium Is Induced by α2-Adrenergic Stimulation

机译：α2-肾上腺素能刺激诱导巨噬细胞对鸟分枝杆菌的抗性。

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The ability of macrophages to control the growth of microorganisms is increased by macrophage activation. Previously, it was shown that epinephrine activated mouse macrophages to resist the growth of Mycobacterium avium via α2-adrenergic stimulation. In the present study, we show that the α2-adrenergic agonist (α2-agonist) clonidine induced resistance to M. avium growth in the RAW264.7 mouse macrophage cell line. The ability of catecholamines to induce resistance to mycobacteria was specific to α2-adrenergic stimulation, as α1-, β1-, and β2-agonists had no effect. Receptor signaling through Gi proteins was required. A G-protein antagonist specific for the α subunits of the Go/Gi family blocked the increased resistance induced by clonidine, while a Gs-protein antagonist was without effect. Both nitric oxide (NO) production and superoxide (O2?) production were required for the increased resistance to M. avium growth induced by clonidine. Although NO production was required, clonidine did not increase the level of NO in M. avium-infected cells. Since NO and O2? interact to produce peroxynitrite (ONOO?), we examined whether ONOO? mediates the increased resistance to M. avium induced by clonidine. 5,10,15,20-Tetrakis(4-sulfonatophenyl)prophyrinato iron (III) chloride (FeTPPS), a specific scavenger of ONOO?, inhibited the effect of clonidine on M. avium growth. Clonidine also increased the production of ONOO? in M. avium-infected RAW264.7 cells, as measured by the oxidation of 123-dihydrorhodamine and the production of nitrated tyrosine residues. We therefore conclude that α2-adrenergic stimulation activates macrophages to resist the growth of M. avium by enhancing the production of ONOO?.
机译：巨噬细胞激活可增强巨噬细胞控制微生物生长的能力。以前的研究表明，肾上腺素通过α 2 -肾上腺素能刺激小鼠巨噬细胞抵抗鸟分枝杆菌的生长。在本研究中，我们表明α 2 -肾上腺素能激动剂（α 2 -激动剂）可乐定诱导对 M的抗性。 RAW264.7小鼠巨噬细胞系中鸟卵的生长。儿茶酚胺诱导对分枝杆菌的抗性的能力对α 2 -肾上腺素能刺激具有特异性，如α 1 -，β 1 -和β。 2 -激动剂无效。需要通过Gi蛋白的受体信号传导。对Go / Gi家族的α亚基具有特异性的G蛋白拮抗剂可以阻止可乐定诱导的耐药性增加，而Gs蛋白拮抗剂则没有作用。一氧化氮（NO）的产生和超氧化物（O 2 ？）的产生都需要增加对 M的抗性。可乐定诱导鸟卵生长。尽管需要产生NO，但可乐定不会增加 M中的NO水平。鸟感染的细胞。由于NO和O 2 ？相互作用产生过氧亚硝酸盐（ONOO ？），因此我们检查了ONOO ？是否介导了亚硝酸盐。对 M的抵抗力增强。可乐定引起的鸟卵。 5,00,15,20-四（4-磺酰基苯基）原卟啉铁氯化物（FeTPPS）是ONOO ？的特定清除剂，抑制了可乐定对 M的作用。鸟类生长。可乐定还增加了 M中ONOO ？的产生。通过123-二氢罗丹明的氧化作用和硝酸化酪氨酸残基的产生来测量被avium 感染的RAW264.7细胞。因此，我们得出结论，α 2 -肾上腺素能刺激激活巨噬细胞以抵抗 M的生长。增强了ONOO ？的产量。

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