Lack of flagella disadvantages Salmonella enterica serovar Enteritidis during the early stages of infection in the rat

Robertson, Jeanette M.C.; Duncan, Michelle; Allen‐Vercoe, Emma; Woodward, Martin J.; Flint, Harry J.; Grant, George

doi:10.1099/jmm.0.04901-0

Cited by 56 publications

(39 citation statements)

References 46 publications

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“…Bacterial flagellin is a virulence factor of S. enterica. Strains of Salmonella deficient in flagellin can exhibit defects in colonization and tissue invasion, as well as invasion of macrophages and epithelial cells in vitro [2,3].…”

Section: Introductionmentioning

confidence: 99%

Activation of NF-κB-dependent gene expression by Salmonella flagellins FliC and FljB

Simon

Samuel

2007

Biochemical and Biophysical Research Communications

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Bacterial flagellin is recognized by Toll-like receptor (TLR5) and activates NF-κB which leads to the induction of proinflammatory gene expression. Salmonella expresses two flagellin proteins, FliC and FljB. We purified FliC and FljB and examined the ability of the Salmonella flagellins to activate the NF-κB transcription factor in human embryonic kidney cells. We found that FliC and FljB as purified proteins possessed a comparable specific activity for activation of NF-κB-dependent gene expression in HEK293 cells. We also determined the ability of UV-inactivated bacteria, both wildtype and fliC and fljB mutant strains, to activate NF-κB. Wild-type fliC + /fljB + Salmonella and the fliC + /fljB − mutant strain were robust activators, whereas the fliC − /fljB + and flhC − mutant strains were very poor activators. The NF-κB activation capacity of bacterial strains correlated with their flagellin expression level. Finally, Salmonella cell wall-associated polymeric flagellin displayed greatly reduced ability to activate NF-κB compared to purified monomeric flagellin.

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Section: Introductionmentioning

confidence: 99%

Activation of NF-κB-dependent gene expression by Salmonella flagellins FliC and FljB

Simon

Samuel

2007

Biochemical and Biophysical Research Communications

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“…The mechanism for this phenomenon is still unknown. Many studies have shown the importance of flagella for virulence of S. enterica serovars (87,182,188,197), although the specific aspect of flagellar function that contributes to virulence remains unclear.…”

Section: Fliamentioning

confidence: 99%

Alternative Sigma Factors and Their Roles in Bacterial Virulence

Kazmierczak

Wiedmann

Boor

2005

Microbiol Mol Biol Rev

320

317

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SUMMARY Sigma factors provide promoter recognition specificity to RNA polymerase holoenzyme, contribute to DNA strand separation, and then dissociate from the core enzyme following transcription initiation. As the regulon of a single sigma factor can be composed of hundreds of genes, sigma factors can provide effective mechanisms for simultaneously regulating expression of large numbers of prokaryotic genes. One newly emerging field is identification of the specific roles of alternative sigma factors in regulating expression of virulence genes and virulence-associated genes in bacterial pathogens. Virulence genes encode proteins whose functions are essential for the bacterium to effectively establish an infection in a host organism. In contrast, virulence-associated genes can contribute to bacterial survival in the environment and therefore may enhance the capacity of the bacterium to spread to new individuals or to survive passage through a host organism. As alternative sigma factors have been shown to regulate expression of both virulence and virulence-associated genes, these proteins can contribute both directly and indirectly to bacterial virulence. Sigma factors are classified into two structurally unrelated families, the σ70 and the σ54 families. The σ70 family includes primary sigma factors (e.g., Bacillus subtilis σA) as well as related alternative sigma factors; σ54 forms a distinct subfamily of sigma factors referred to as σN in almost all species for which these proteins have been characterized to date. We present several examples of alternative sigma factors that have been shown to contribute to virulence in at least one organism. For each sigma factor, when applicable, examples are drawn from multiple species.

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“…Salmonella lacking flagellin expression were initially reported to have reduced virulence (43,44), but this finding was later refuted (45,46). The most recent data indicate that nonflagellated bacteria have reduced virulence in cell culture experiments, but are virulent, or only have slightly reduced virulence in vivo (47,48). However, the effect of Salmonella flagellin overexpression has not been examined.…”

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confidence: 99%

SalmonellaFlagellin Induces Bystander Activation of Splenic Dendritic Cells and Hinders Bacterial Replication In Vivo

Salazar-González

Srinivasan

Griffin

et al. 2007

The Journal of Immunology

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Bacterial flagellin is a target of innate and adaptive immune responses during Salmonella infection. Intravenous injection of Salmonella flagellin into C57BL/6 mice induced rapid IL-6 production and increased expression of activation markers by splenic dendritic cells. CD11b+, CD8α+, and plasmacytoid dendritic cells each increased expression of CD86 and CD40 in response to flagellin stimulation, although CD11b+ dendritic cells were more sensitive than the other subsets. In addition, flagellin caused the rapid redistribution of dendritic cells from the red pulp and marginal zone of the spleen into the T cell area of the white pulp. Purified splenic dendritic cells did not respond directly to flagellin, indicating that flagellin-mediated activation of splenic dendritic cells occurs via bystander activation. IL-6 production, increased expression of activation markers, and dendritic cell redistribution in the spleen were dependent on MyD88 expression by bone marrow-derived cells. Avoiding this innate immune response to flagellin is important for bacterial survival, because Salmonella-overexpressing recombinant flagellin was highly attenuated in vivo. These data indicate that flagellin-mediated activation of dendritic cells is rapid, mediated by bystander activation, and highly deleterious to bacterial survival.

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Lack of flagella disadvantages Salmonella enterica serovar Enteritidis during the early stages of infection in the rat

Cited by 56 publications

References 46 publications

Activation of NF-κB-dependent gene expression by Salmonella flagellins FliC and FljB

Activation of NF-κB-dependent gene expression by Salmonella flagellins FliC and FljB

Alternative Sigma Factors and Their Roles in Bacterial Virulence

SalmonellaFlagellin Induces Bystander Activation of Splenic Dendritic Cells and Hinders Bacterial Replication In Vivo

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