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首页> 外文期刊>Infection and immunity >Intracellular survival and replication of Erysipelothrix rhusiopathiae within murine macrophages: failure of induction of the oxidative burst of macrophages.
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Intracellular survival and replication of Erysipelothrix rhusiopathiae within murine macrophages: failure of induction of the oxidative burst of macrophages.

机译：鼠巨噬细胞内红斑丹毒菌的细胞内存活和复制：巨噬细胞氧化爆发诱导失败。

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We investigated the ability of a virulent wild-type parent strain and acapsular avirulent transposon mutants to enter and survive intracellularly within murine peritoneal macrophages. In the presence of normal or immune serum, the parent and mutant strains were both ingested; however, the number of ingested bacteria was three- to fourfold greater in the case of mutant strains than in the case of the parent strain. The parent strain, but not the mutant strains, survived and replicated intracellularly when ingested in the presence of normal serum, whereas both the parent and the mutant strains were readily killed when ingested in the presence of immune serum. To further investigate the mechanism by which the parent strain can survive and replicate within macrophages, we studied the oxidative burst response of macrophages to these strains by measuring chemiluminescence and intracellular reduction of Nitro Blue Tetrazolium dye. Challenge exposure of macrophages with either the parent strain preopsonized with immune serum or the mutant strains preopsonized with normal or immune serum induced a strong oxidative burst, whereas the level was very low when the parent strain was preopsonized with normal serum. Phagocytosis of either the parent strain, in the presence of immune serum, or the mutant strains, in the presence of normal or immune serum, by macrophages reduced large amounts of intracellular Nitro Blue Tetrazolium, whereas minimal amounts were reduced by the parent strain in the presence of normal serum. These results suggest that virulent E. rhusiopathiae can survive and subsequently replicate within murine macrophages when ingested in the presence of normal serum and that the reduced production of reactive oxidative metabolites by macrophages may, in part, be responsible for this occurrence.
机译：我们调查了有毒的野生型亲本菌株和无荚膜无毒转座子突变体进入并在鼠腹膜巨噬细胞内生存的能力。在正常或免疫血清存在的情况下，母本和突变株均被摄入。然而，突变菌株的摄取细菌数量比亲本菌株的摄取细菌数量高三到四倍。当在正常血清中摄取时，亲本菌株而非突变体菌株存活并在细胞内复制，而当在免疫血清中摄取时，亲本和突变体菌株均容易被杀死。为了进一步研究亲本菌株可以在巨噬细胞中存活和复制的机制，我们通过测量化学发光和硝基蓝四唑染料的细胞内还原研究了巨噬细胞对这些菌株的氧化爆发反应。用免疫血清预先调理过的亲本菌株或用正常或免疫血清预先调理过的突变菌株对巨噬细胞的挑战暴露诱导了强烈的氧化爆发，而当用正常血清预调理了亲本菌株时，该水平非常低。巨噬细胞在存在免疫血清的情况下对母本菌株的吞噬作用，或在正常或免疫血清存在下的突变体对巨噬细胞的吞噬作用降低了细胞内硝基蓝四唑的量，而母本菌株在巨噬细胞中则减少了少量。存在正常血清。这些结果表明，当在正常血清中摄入时，强毒性的风疹病原体可以存活并随后在鼠巨噬细胞内复制，并且巨噬细胞反应性氧化代谢产物的产生减少可能部分是造成这种情况的原因。

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