Natural History of Oral Salmonella dublin Infection in BALB/c Mice: Effect of an 80-Kilobase-Pair Plasmid on Virulence

Heffernan, Edwin J.; Fierer, Joshua; Chikami, Gary; Guiney, Donald G.

doi:10.1093/infdis/155.6.1254

Cited by 103 publications

(83 citation statements)

References 24 publications

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“…Furthermore, a low inoculum more accurately re¯ects the in vivo situation. Viable bacteria in the livers and spleens of infected mice increase 10 4 -to 10 5 -fold from an initial load of only a few hundred organisms after oral infection (Heffernan et al, 1987). Our results are compatible with an earlier in vivo study using a different temperature-sensitive plasmid to demonstrate that the spv genes appeared to increase the intracellular growth rate of S. typhimurium in the spleen (Gulig and Doyle, 1993).…”

Section: Discussionsupporting

confidence: 90%

The Salmonella virulence plasmid spv genes are required for cytopathology in human monocyte-derived macrophages

et al. 2000

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SummaryThe pathogenesis of serious systemic Salmonella infections is characterized by survival and proliferation of bacteria inside macrophages. Infection of human monocyte-derived macrophages in vitro with S. typhimurium or S. dublin produces cytopathology characterized by detachment of cells that contain large numbers of proliferating bacteria. This cytopathology is dependent on the expression of the bacterial spv genes, a virulence locus previously shown to markedly enhance the ability of Salmonella to produce systemic disease. After 24 h of infection, macrophage cultures contain two populations of bacteria: (i) proliferating organisms present in a detached cell fraction; and (ii) a static bacterial population in macrophages remaining attached to the culture well. Mutations in either the essential transcriptional activator SpvR or the key SpvB protein markedly reduce the cytopathic effect of Salmonella infection. The spvdependent cytopathology in macrophages exhibits characteristics of apoptosis, with release of nucleosomes into the cytoplasm, nuclear condensation and DNA fragmentation. The current ®ndings suggest that the mechanism of the spv effect is through induction of increased cytopathology in host macrophages.

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Section: Discussionsupporting

confidence: 90%

The Salmonella virulence plasmid spv genes are required for cytopathology in human monocyte-derived macrophages

et al. 2000

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“…Dublin virulence plasmid genes (sp ) have been found to be strongly expressed when the organism is within eucaryotic cells and to be regulated by both SpvR and RpoS [135,136]. The sp genes are required for survival and replication of Dublin within bovine monocytes [131,137], and experimental Dublin infections have shown that these virulence genes are necessary for the development of systemic salmonellosis in both the bovine and murine hosts but do not affect the capability of Dublin to colonize the intestine, to invade PP or to cause diarrhoea in cattle [138,139]. Alternatively, enteric inflammation appears to be due to Dublin adhesion to the epithelial cells and is mediated by activation of the proinflammatory genes transcription factor NF-kB and chemokine (i.e.…”

Section: Dublinmentioning

confidence: 99%

Host adapted serotypes of Salmonella enterica

et al. 2000

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Salmonella constitutes a genus of zoonotic bacteria of worldwide economic and health importance. The current view of salmonella taxonomy assigns the members of this genus to two species: S. enterica and S. bongori. S. enterica itself is divided into six subspecies, enterica, salamae, arizonae, diarizonae, indica, and houtenae, also known as subspecies I, II, IIIa, IIIb, IV, and VI, respectively [1]. Members of Salmonella enterica subspecies enterica are mainly associated with warm-blooded vertebrates and are usually transmitted by ingestion of food or water contaminated by infected faeces. The pathogenicity of most of the distinct serotypes remains undefined, and even within the most common serotypes, many questions remain to be answered regarding the interactions between the organism and the infected host.Salmonellosis manifests itself in three major forms: enteritis, septicaemia, and abortion, each of which may be present singly or in combination, depending on both the serotype and the host involved. Although currently over 2300 serovars of Salmonella are recognized, only about 50 serotypes are isolated in any significant numbers as human or animal pathogens [2, 3] and they all belong to subspecies enterica. Of these, most cause acute gastroenteritis characterized by a short incubation period and a severe systemic disease in man or animals, characterized by septicaemia, fever and/or abortion, and such serotypes are often associated with one or few host species [4–6].It is the intention of this review to present a summary of current knowledge of these host-adapted serotypes of S. enterica. The taxonomic relationships between the serotypes will be discussed together with a comparison of the pathology and pathogenesis of the disease that they cause in their natural host(s). Since much of our knowledge on salmonellosis is based on the results of work on Typhimurium, this serotype will often be used as the baseline in discussion. It is hoped that an appreciation of the differences that exist in the way these serotypes interact with the host will lead to a greater understanding of the complex host–parasite relationship that characterizes salmonella infections.

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“…or i.v. in a lateral tail vein in 0.1 ml PBS or orally by gavage in 0.1 ml 0.1 M NaHCO 3 (23). Mice were sacrificed at intervals, and the tissues were removed sterilely, homogenized, and then diluted in saline for quantitative cultures as previously described (23).…”

Section: Infectionmentioning

confidence: 99%

The Role of Lipopolysaccharide Binding Protein in Resistance to Salmonella Infections in Mice

Fierer

Swancutt

Heumann

et al. 2002

The Journal of Immunology

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Polymorphonuclear leukocytes (PMN) and LPS-binding protein (LBP) are both components of the innate immune system. LBP is a plasma protein that binds to lipid A and enhances the biological activity of LPS 100- to 1000-fold. Recently it was reported that LBP-deficient mice are more susceptible to Salmonella typhimurium infection. Here we report that LBP KO mice are more susceptible to Salmonella peritonitis, but not to oral or i.v. infection. LBP knockout (KO) mice responded normally to i.p. injections of Staphylococcus aureus and casein, but not to i.p. injection of S. typhimurium or Salmonella LPS. Mice with a mutation in Toll-like receptor 4 (C3H/HeJ) have a similar defect in PMN chemotaxis. In normal mice S. typhimurium stimulated production of the CXC chemokines macrophage inflammatory protein-2 and cytokine-induced neutrophil chemoattractant, but levels of cytokine-induced neutrophil chemoattractant and macrophage inflammatory protein-2 were greatly reduced in the LBP KO mice. LBP KO mice pretreated with casein to attract PMN in an LBP-independent manner were more resistant to Salmonella infection, but neutropenic mice were not protected by casein. Splenic TNF-α mRNA levels were also lower in LBP KO than in control mice infected with Salmonella. Since TNF-α can activate PMN, LBP KO mice may have both fewer and less active PMN in the first few hours after Salmonella are injected, making LBP KO mice more susceptible. This work confirms the importance of PMN in resistance to Salmonella infections and shows that this is facilitated by LBP.

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Natural History of Oral Salmonella dublin Infection in BALB/c Mice: Effect of an 80-Kilobase-Pair Plasmid on Virulence

Cited by 103 publications

References 24 publications

The Salmonella virulence plasmid spv genes are required for cytopathology in human monocyte-derived macrophages

The Salmonella virulence plasmid spv genes are required for cytopathology in human monocyte-derived macrophages

Host adapted serotypes of Salmonella enterica

The Role of Lipopolysaccharide Binding Protein in Resistance to Salmonella Infections in Mice

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