Peroxynitrite enhances the ability of Salmonella dublin to invade T84 monolayers
Peroxynitrite enhances the ability of Salmonella dublin to invade T84 monolayers
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DOI：
10.1097/00024382-200207000-00017
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发表时间：
2002-07-01
期刊：
影响因子：
3.1
通讯作者：
Madsen, KL
中科院分区：
文献类型：
--
作者：
Cornish, AS;Jijon, H;Madsen, KL
在肠中，上皮细胞持续产生和分泌低水平的一氧化氮（NO）。沙门氏菌通过对环境刺激的反应侵入上皮。本研究的目的是确定活性氮中间体（RNI）对S的影响。都柏林和S.鼠伤寒沙门氏菌，T-84上皮单层的生长和侵袭。7-硝基吲唑（7-NI）或N-G-单甲基-L-精氨酸单乙酸酯（L-NMMA）可抑制细胞内NO的生成，亚铁血红蛋白或尿酸盐可清除细胞外NO和过氧亚硝基阴离子。研究了过氧化亚硝酸根（ONOO-）、通过NO和超氧阴离子释放ONOO-的3-吗啉基-悉尼酮亚胺（SIN-1）、仅释放NO的精胺NONOate以及黄嘌呤氧化酶和蝶呤产生的超氧阴离子对S.都柏林和S.检测鼠伤寒的生长和侵袭。抑制NO合成和清除细胞外NO或过氧亚硝酸盐还原S。都柏林侵入T-84单层并增强细菌生长。S.都柏林到ONOO-和SIN-1增加随后的细菌侵入T84单层。相反，暴露于精胺NONOate或超氧化物对S。都柏林入侵相反，S.用NO供体预处理不影响鼠伤寒侵袭。结论：S.都柏林到ONOO-增强细菌侵入上皮细胞的能力。这些结果表明，管腔ONOO-可能有一个新的作用，作为一个细胞外信号之间的侵入性细菌和上皮细胞。
In the intestine, epithelial cells continually produce and secrete low levels of nitric oxide (NO). Salmonella sp. invade epithelium by responding to environmental stimuli. The aims of this study were to determine the effect of reactive nitrogen intermediates (RNIs) on S. dublin and S. typhimurium, growth and invasion of T-84 epithelial monolayers. Intracellular NO formation was inhibited by 7-nitroindazole (7-NI) or N-G-monomethyl-L-arginine, monoacetate (L-NMMA); extracellular NO and peroxynitrite were scavenged with ferro-hemoglobin or urate. The effect of authentic peroxynitrite (ONOO-); 3-morpholino-sydnonimine (SIN-1), which releases ONOO- via NO and superoxide; spermine NONOate, which releases only NO; or superoxide generated by xanthine oxidase and pterin on S. dublin and S. typhimurium growth and invasion were examined. Inhibition of NO synthesis and scavenging of extracellular NO or peroxynitrite reduced S. dublin invasion into T-84 monolayers and enhanced bacterial growth. Pre-exposure of S. dublin to ONOO- and SIN-1 increased subsequent bacterial invasion into T84 monolayers. Conversely, exposure of bacteria to spermine NONOate or superoxide did not affect S. dublin invasion. In contrast, S. typhimurium invasion was not affected by pre-treatment with NO donors. In conclusion, exposure of S. dublin to ONOO- enhances the ability of the bacteria to invade epithelial cells. These results suggest that luminal ONOO- may have a novel role as an extracellular signal between invasive bacteria and epithelial cells.