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沙门氏菌血清型宿主特异性致病的一种可能机制。

A possible mechanism for host-specific pathogenesis of Salmonella serovars.

作者信息

Ishibashi Y, Arai T

机构信息

Department of Microbiology, Meiji College of Pharmacy, Tokyo, Japan.

出版信息

Microb Pathog. 1996 Dec;21(6):435-46. doi: 10.1006/mpat.1996.0074.

DOI:10.1006/mpat.1996.0074
PMID:8971684
Abstract

We have identified the complement receptors on human and murine macrophages involved in the recognition of Salmonella serovars, and investigated their relevance to the intracellular survival. S. typhi was capable of surviving within human monocyte-derived macrophages, whereas S. typhimurium was not. Conversely, S. typhimurium, but not S. typhi, resisted intracellular killing by murine macrophages, demonstrating that the intracellular survival of Salmonella serovars is host-dependent. In the presence of serum opsonin, human monocyte-derived macrophages recognized S. typhi and S. typhimurium via complement receptor type 1 (CR1) and type 3 (CR3), respectively. In contrast, murine macrophages recognized S. typhi and S. typhimurium via CR3 and CR1, respectively. These findings demonstrate that the intracellular fate of Salmonella serovars following phagocytosis may depend on the type of complement receptors involved in their recognition, in that CR1-mediated recognition is closely correlated to subsequent intracellular survival. The Tn5 insertion mutant of S. typhimurium which lacks the ability to interact with CR1 was sensitive to intracellular killing by murine macrophages in vitro, and was much less virulent to mice in vivo, confirming the relevance of CR1-mediated bacterial recognition to the pathogenicity of S. typhimurium for mice. These results suggest that selective recognition of Salmonella serovars through CR1 may lead to their subsequent intracellular survival, and is responsible for the host-specific pathogenesis of Salmonella serovars.

摘要

我们已经鉴定出参与识别沙门氏菌血清型的人和鼠巨噬细胞上的补体受体,并研究了它们与细胞内存活的相关性。伤寒沙门氏菌能够在人单核细胞衍生的巨噬细胞内存活,而鼠伤寒沙门氏菌则不能。相反,鼠伤寒沙门氏菌而非伤寒沙门氏菌能抵抗鼠巨噬细胞的细胞内杀伤,这表明沙门氏菌血清型的细胞内存活是宿主依赖性的。在血清调理素存在的情况下,人单核细胞衍生的巨噬细胞分别通过1型补体受体(CR1)和3型补体受体(CR3)识别伤寒沙门氏菌和鼠伤寒沙门氏菌。相比之下,鼠巨噬细胞分别通过CR3和CR1识别伤寒沙门氏菌和鼠伤寒沙门氏菌。这些发现表明,吞噬作用后沙门氏菌血清型的细胞内命运可能取决于参与其识别的补体受体类型,因为CR1介导的识别与随后的细胞内存活密切相关。缺乏与CR1相互作用能力的鼠伤寒沙门氏菌Tn5插入突变体在体外对鼠巨噬细胞的细胞内杀伤敏感,并且在体内对小鼠的毒性要小得多,这证实了CR1介导的细菌识别与鼠伤寒沙门氏菌对小鼠的致病性相关。这些结果表明,通过CR1对沙门氏菌血清型的选择性识别可能导致其随后的细胞内存活,并导致沙门氏菌血清型的宿主特异性发病机制。

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