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首页> 外文期刊>Infection and immunity >A Superoxide-Hypersusceptible Salmonella enterica Serovar Typhimurium Mutant Is Attenuated but Regains Virulence in p47phox?/? Mice
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A Superoxide-Hypersusceptible Salmonella enterica Serovar Typhimurium Mutant Is Attenuated but Regains Virulence in p47phox?/? Mice

机译：超氧化物歧化肠炎沙门氏菌鼠伤寒沙门氏菌突变体减弱，但恢复了p47phox？/？的毒力。老鼠

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Salmonella enterica serovar Typhimurium is a gram-negative, facultative intracellular pathogen that predominantly invades mononuclear phagocytes and is able to establish persistent infections. One of the innate defense mechanisms of phagocytic cells is the production of reactive oxygen species, including superoxide. S. enterica serovar Typhimurium has evolved mechanisms to resist such radicals, and these mechanisms could be decisive in its ability to survive and replicate within macrophages. Recently, we described a superoxide-hypersusceptible S. enterica serovar Typhimurium mutant strain, DLG294, that carries a transposon in sspJ, resulting in the lack of expression of SspJ, which is necessary for resistance against superoxide and replication within macrophages. Here we show that DLG294, which is a 14028s derivative, hardly induced any granulomatous lesions in the livers upon subcutaneous infection of C3H/HeN (Ityr) mice with 3 × 104 bacteria and that its bacterial counts were reduced by 3 log units compared to those of wild-type S. enterica serovar Typhimurium 14028s on day 5 after infection. In contrast, DLG294 replicated like wild-type S. enterica serovar Typhimurium 14028s and induced a phenotypically similar liver pathology in p47phox?/? mice, which are deficient in the p47phox subunit of the NADPH oxidase complex and which do not produce superoxide. Consistent with these results, DLG294 reached bacterial counts identical to those of wild-type S. enterica serovar Typhimurium 14028s in bone marrow-derived macrophages from p47phox?/? mice and in X-CGD PLB-985 cells at 24 h after challenge. These results indicate that SspJ plays a role in the bacterium's resistance to oxidative stress and in the survival and replication of S. enterica serovar Typhimurium both in vitro and in vivo.
机译：鼠伤寒沙门氏菌是一种革兰氏阴性，兼性的细胞内病原体，主要侵袭单核吞噬细胞并能够持续感染。吞噬细胞的先天防御机制之一是产生活性氧，包括超氧化物。 S。肠伤寒鼠伤寒沙门氏菌已发展出抵抗此类自由基的机制，这些机制可能决定其在巨噬细胞中存活和复制的能力。最近，我们描述了超氧化物敏感性超高的 S。在 sspJ 中带有转座子的肠炎血清型鼠伤寒突变株DLG294，导致SspJ的表达缺失，这对于抵抗超氧化物歧化和在巨噬细胞内复制是必需的。在这里，我们显示DLG294是一种14028s衍生物，在用3×10 4 ）小鼠后几乎不会在肝脏中引起肉芽肿性病变。细菌，其细菌数量与野生型 S相比减少了3个对数单位。感染后第5天出现肠型鼠伤寒沙门氏菌14028s。相反，DLG294像野生型 S一样复制。鼠血清型鼠伤寒沙门氏菌14028s，并在p47 phox？/？小鼠中产生表型相似的肝脏病理，这是NADPH氧化酶复合体的p47 phox 亚基缺乏的原因并且不会产生超氧化物。与这些结果一致，DLG294的细菌计数与野生型 S相同。攻击后24 h，p47 phox？/？小鼠骨髓来源的巨噬细胞和X-CGD PLB-985细胞中的肠炎血清型鼠伤寒14028s。这些结果表明，SspJ在细菌对氧化应激的抗性以及 S的存活和复制中起作用。肠球菌血清和鼠伤寒。

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