In vivo, fliC expression by Salmonella enterica serovar Typhimurium is heterogeneous, regulated by ClpX, and anatomically restricted

Cummings, Lisa A.; Wilkerson, W. David; Bergsbaken, Tessa; Cookson, Brad T.

doi:10.1111/j.1365-2958.2006.05271.x

Cited by 167 publications

(199 citation statements)

References 73 publications

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“…There are several reports that the expression of FliC is downregulated in Salmonella-infected macrophages or during Salmonella infection in mice (Alaniz et al, 2006;Cummings et al, 2006;Eriksson et al, 2003). However, our data showed that FliC was detected in about 70 % of macrophages infected with the wild-type strain but almost not at all in macrophages infected with the spiC mutant.…”

Section: Discussioncontrasting

confidence: 55%

Salmonella virulence factor SpiC is involved in expression of flagellin protein and mediates activation of the signal transduction pathways in macrophages

Uchiya

Nikai

2008

Microbiology

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Section: Discussioncontrasting

confidence: 55%

Salmonella virulence factor SpiC is involved in expression of flagellin protein and mediates activation of the signal transduction pathways in macrophages

Uchiya

Nikai

2008

Microbiology

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“…For example, integration host factor was found to repress the expression of flagellin in EPEC and EHEC when grown in DMEM (45). Similarly, studies of other bacterial pathogens suggest that while flagellin expression may occur at early stages of infection, or at specific tissue sites, flagellin expression may be reduced or even absent at later stages of infection, as was recently described for Salmonella enterica serovar Typhimurium (11).…”

Section: Discussionmentioning

confidence: 86%

Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

Khan

Bouzari

et al. 2008

Infect Immun

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Enteropathogenic Escherichia coli (EPEC) and the murine pathogen Citrobacter rodentium belong to the attaching and effacing (A/E) family of bacterial pathogens. These noninvasive bacteria infect intestinal enterocytes using a type 3 secretion system (T3SS), leading to diarrheal disease and intestinal inflammation. While flagellin, the secreted product of the EPEC fliC gene, causes the release of interleukin 8 (IL-8) from epithelial cells, it is unclear whether A/E bacteria also trigger epithelial inflammatory responses that are FliC independent. The aims of this study were to characterize the FliC dependence or independence of epithelial inflammatory responses to direct infection by EPEC or C. rodentium. Following infection of Caco-2 intestinal epithelial cells by wild-type and ⌬fliC EPEC, a rapid activation of several proinflammatory genes, including those encoding IL-8, monocyte chemoattractant protein 1, macrophage inflammatory protein 3␣ (MIP3␣), and ␤-defensin 2, occurred in a FliC-dependent manner. These responses were accompanied by mitogen-activated protein kinase activation, as well as the Toll-like receptor 5 (TLR5)-dependent activation of NF-B. At later infection time points, a subset of these proinflammatory genes (IL-8 and MIP3␣) was also induced in cells infected with ⌬fliC EPEC. The nonmotile A/E pathogen C. rodentium also triggered similar innate responses through a TLR5-independent but partially NF-B-dependent mechanism. Moreover, the EPEC FliC-independent responses were increased in the absence of the locus of enterocyte effacement-encoded T3SS, suggesting that translocated bacterial effectors suppress rather than cause the FliC-independent inflammatory response. Thus, we demonstrate that infection of intestinal epithelial cells by A/E pathogens can trigger an array of proinflammatory responses from epithelial cells through both FliC-dependent and -independent pathways, expanding our understanding of the innate epithelial response to infection by these pathogens.

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“…When the pathogen Salmonella enterica serovar Typhimurium is grown under homogenous conditions in rich media, transcription of the flagellin monomer fliC is bistable, with well-defined subpopulations of fliC-OFF and fliC-ON cells (3). In this organism, a three-class transcriptional cascade orders the production of flagellar proteins (4).…”

mentioning

confidence: 99%

Regulation of phenotypic heterogeneity permits Salmonella evasion of the host caspase-1 inflammatory response

Stewart¹,

Cummings

Johnson

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Sensing and adapting to the environment is one strategy by which bacteria attempt to maximize fitness in an unpredictable world; another is the stochastic generation of phenotypically distinct subgroups within a genetically clonal population. In culture, Salmonella Typhimurium populations are bistable for the expression of flagellin. We report that YdiV controls this expression pattern by preventing transcription of the sigma factor that recruits RNA polymerase to the flagellin promoter. Bistability ensues when the sigma factor is repressed in a subpopulation of cells, resulting in two phenotypes: flagellin expressors and flagellin nonexpressors. Although the ability to swim is presumably a critical survival trait, flagellin activates eukaryotic defense pathways, and Salmonella restrict the production of flagellin during systemic infection. Salmonella mutants lacking YdiV are unable to fully repress flagellin at systemic sites, rendering them vulnerable to caspase-1 mediated colonization restriction. Thus, a regulatory mechanism producing bistability also impacts Salmonella virulence.

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In vivo, fliC expression by Salmonella enterica serovar Typhimurium is heterogeneous, regulated by ClpX, and anatomically restricted

Abstract: Summary FliC is a natural antigen recognized by the innate and adaptive immune systems during

Cited by 167 publications

References 73 publications

Salmonella virulence factor SpiC is involved in expression of flagellin protein and mediates activation of the signal transduction pathways in macrophages

Salmonella virulence factor SpiC is involved in expression of flagellin protein and mediates activation of the signal transduction pathways in macrophages

Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

Regulation of phenotypic heterogeneity permits Salmonella evasion of the host caspase-1 inflammatory response

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