Transposon insertion mutagenesis of a genetic region encoding serum resistance in an 80 kb plasmid of Salmonella dublin

Terakado, Nobuaki; Ushijima, Toshihiro; Samejima, Toshiya; Ito, Hiroya; Hamaoka, Toshiyuki; Murayama, Somay Yamagata; Kawahara, Kazuyoshi; Danbara, Hirofumi

doi:10.1099/00221287-136-9-1833

Cited by 8 publications

(2 citation statements)

References 35 publications

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“…LPS seems to play multiple roles in Salmonella infection of a host. One of the contributions of the molecule to virulence is the protection of the bacterium from serum-mediated killing as well as from the hostile intracellular environment of the phagolysosome (7,18,21,56,58,60,61). In addition, it has been established that LPS induces the production of cytokines (12).…”

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confidence: 99%

Study of the role of the htrB gene in Salmonella typhimurium virulence

et al. 1997

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We have undertaken a study to investigate the contribution of the htrB gene to the virulence of pathogenic Salmonella typhimurium. An htrB::mini-Tn10 mutation from Escherichia coli was transferred by transduction to the mouse-virulent strain S. typhimurium SL1344 to create an htrB mutant. The S. typhimurium htrB mutant was inoculated into mice and found to be severely limited in its ability to colonize organs of the lymphatic system and to cause systemic disease in mice. A variety of experiments were performed to determine the possible reasons for this loss of virulence. Serum killing assays revealed that the S. typhimurium htrB mutant was as resistant to killing by complement as the wild-type strain. However, macrophage survival assays revealed that the S. typhimurium htrB mutant was more sensitive to the intracellular environment of murine macrophages than the wild-type strain. In addition, the bioactivity of the lipopolysaccharide (LPS) of the htrB mutant was reduced compared to that of the LPS from the parent strain as measured by both a Limulus amoebocyte lysate endotoxin quantitation assay and a tumor necrosis factor alpha bioassay. These results indicate that the htrB gene plays a role in the virulence of S. typhimurium.

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Study of the role of the htrB gene in Salmonella typhimurium virulence

et al. 1997

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“…These pathogenic bacteria possess many virulence determinants which they use to establish infection of a host. For example, lipopolysaccharide provides protection against host killing mechanisms (52,54,56). Additionally, the bacteria possess a set of genes that encode a type III secretion system which enables the bacteria to penetrate the membrane of host cells (1,24,27,29,35,38,42).…”

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Inhibition ofSalmonella typhimuriumInvasion by Host Cell Expression of Secreted Bacterial Invasion Proteins

Carlson

Jones

1998

Infect Immun

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Pathogenic Salmonella species initiate infection of a host by inducing their own uptake into intestinal epithelial cells. An invasive phenotype is conferred to this pathogen by a number of proteins that are components of a type III secretion system. During the invasion process, the bacteria utilize this secretion system to release proteins that enter the host cell and apparently interact with unknown host cell components that induce alterations in the actin cytoskeleton. To investigate the role of secreted proteins as direct modulators of invasion, we have evaluated the ability of Salmonella typhimurium to enter mammalian cells that express portions of theSalmonella invasion proteins SipB and SipC. Plasma membrane localization of SipB and SipC was achieved by fusing carboxyl- and amino-terminal portions of each invasion protein to the intracellular carboxyl-terminal tail of a membrane-bound eukaryotic receptor. Expression of receptor chimeras possessing the carboxyl terminus of SipB or the amino terminus of SipC blocked Salmonellainvasion, whereas expression of their chimeric counterparts had no effect on invasion. The effect on invasion was specific forSalmonella since the perturbation of uptake was not extended to other invasive bacterial species. These results suggest that Salmonella invasion can be competitively inhibited by preventing the intracellular effects of SipB or SipC. In addition, these experiments provide a model for examining interactions between bacterial invasion proteins and their host cell targets.

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