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Microb Pathog. 1996 Dec;21(6):435-46.

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

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


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.

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