Enhanced Synthesis of Internalin A inaroMutants ofListeria monocytogenesIndicates Posttranscriptional Control of theinlABmRNA

Stritzker, Jochen; Schoen, Christoph; Goebel, Werner

doi:10.1128/jb.187.8.2836-2845.2005

Cited by 39 publications

(27 citation statements)

References 57 publications

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“…These findings are consistent with previous studies that have demonstrated B -dependent inlA expression in brothgrown L. monocytogenes (24,25,45). Four possible transcriptional start sites have been identified upstream of inlA, including at least one PrfA-dependent and one B -dependent site (24,31,43). The findings reported in the present study highlight the critical contributions of the B -dependent P4 inlA promoter for in vivo gastric internalin A-E-cadherin-mediated infections.…”

Section: Monocytogenessupporting

confidence: 82%

“…(43) reported only three inlA promoters, excluding the P1 promoter described by Lignau et al (31). Thus, the inlA P4, P3, and P2 promoter designations used here are equivalent to the inlA P3, P2, and P1 promoters described by Dramsi et al (8) and Stritzker et al (43). The Ϫ35 and Ϫ10 regions of the B -dependent P4 promoter (24) are boldfaced and underlined.…”

Section: Methodsmentioning

confidence: 99%

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Sigma B Contributes toListeria monocytogenesGastrointestinal Infection but Not to Systemic Spread in the Guinea Pig Infection Model

Garner¹,

Njaa

Wiedmann³

et al. 2006

Infect Immun

116

110

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Contributions of the alternative sigma factorB to Listeria monocytogenes infection were investigated using strains bearing null mutations in sigB, prfA, or inlA or in selected inlA or prfA promoter regions. The ⌬P4 inlA strain, which has a deletion in the B -dependent P4 inlA promoter, and the ⌬sigB strain had significantly reduced invasion efficiencies relative to that of the wild-type strain in the Caco-2 human colorectal epithelial cell line, while the invasion efficiency of a strain bearing a deletion in the partially B dependent P2 prfA promoter region did not differ from that of the wild type. The virulence of the ⌬sigB and ⌬P4 inlA strains was attenuated in intragastrically inoculated guinea pigs, with the ⌬sigB strain showing greater attenuation, while the virulence capacity of the ⌬P2 prfA strain was similar to that of the wild-type strain, suggesting that attenuation of virulence due to the ⌬sigB mutation does not result from loss of B -dependent prfA transcription. Our results show that B -dependent activation of inlA is important for cell invasion and gastrointestinal infection and suggest that B -regulated genes in addition to inlA appear to contribute to gastrointestinal infection. Interestingly, the virulence of the ⌬sigB strain was not attenuated in intravenously infected guinea pigs. We conclude that (i) L. monocytogenes B plays a critical role in invasion of human host cells, (ii) B -mediated contributions to invasion are, in part, due to direct effects on inlA transcription but not on prfA transcription, and (iii) B plays a critical role during the gastrointestinal stage of listeriosis in the guinea pig but is not important for systemic spread of the organism. Listeriosis results from consumption of food contaminated withListeria monocytogenes (40). To cause a human food-borne infection, L. monocytogenes must survive conditions encountered in the oral cavity, the stomach, and the intestine, which include exposure to lysozyme activity, gastric acidity, and bile salts (16). L. monocytogenes can invade the epithelial cells of the small intestine, then spread into mesenteric lymph nodes and disseminate systemically in the blood. Listeriosis is a relatively rare disease among healthy individuals, at least in part because the majority of L. monocytogenes organisms that enter the bloodstream are captured by the Kupffer cells in the liver and are killed by neutrophils (18). Listeriosis occurs predominantly among the immunocompromised, the elderly, and pregnant women and their fetuses (33). In susceptible individuals, L. monocytogenes can cross the bloodbrain barrier to cause central nervous system infections and the placental barrier to cause fetal infections (48). L. monocytogenes cells that escape the antimicrobial activity of the neutrophils can enter hepatocytes or endothelial cells or can be disseminated further to other tissues. Following invasion of nonphagocytic host cells, L. monocytogenes can escape from the host cell vacuole, then replicate intracellularly and spread from cell to cell (6,15...

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Section: Monocytogenessupporting

confidence: 82%

Section: Methodsmentioning

confidence: 99%

Sigma B Contributes toListeria monocytogenesGastrointestinal Infection but Not to Systemic Spread in the Guinea Pig Infection Model

Garner¹,

Njaa

Wiedmann³

et al. 2006

Infect Immun

116

110

View full text Add to dashboard Cite

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“…This indicates that loss of genetic material is not the mechanism of the variation observed and suggests post-transcriptional events, such as differential protein stability and selective protein degradation, may regulate the expression of proteins like IglC. Importantly, regulation of translation has been implicated in the control of genes associated with virulence in several other organisms such as Pseudomonas aeruginosa, Listeria monocytogenes, and Burkholderia cenocepacia [39][40][41][42].…”

Section: Discussionmentioning

confidence: 99%

Modulation of virulence factors in Francisella tularensis determines human macrophage responses

Carlson

Carroll

O’Dee

et al. 2007

Microbial Pathogenesis

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Francisella tularensis, the causative agent of tularemia and Category A biodefense agent, is known to replicate within host macrophages, though the pathogenesis of this organism is incompletely understood. We have isolated a variant of F. tularensis Live Vaccine Strain (LVS) based on colony morphology and its effect on macrophages. Human monocyte-derived macrophages produced more tumor necrosis factor α (TNFα), interleukin (IL)-1β, IL-6, and IL-12 p40 following exposure to the variant, designated the activating variant (ACV). The immunoreactivity of the lipopolysaccharide (LPS) from both LVS and ACV was comparable to the previously described blue variant and was distinct from the gray variant of LVS. We found, however, the soluble protein fractions of LVS and ACV differed. Further investigation using two-dimensional gel electrophoresis demonstrated higher levels of several proteins in the parental LVS isolate. The differentially-expressed proteins featured several associated with virulence in F. tularensis and other pathogens, including intracellular growth locus C (IglC), a σ 54 modulation protein family member (YhbH), and aconitase. ACV reverted to the LVS phenotype, indicated by low cytokine induction and high IglC expression, after growth in a chemically-defined media. These data provide evidence that the levels of virulence factors in F. tularensis are modulated based on culture conditions and that this modulation impacts host responses. This work provides a basis for investigation of Francisella virulence factor regulation and the identification of additional factors, co-regulated with IglC, that affect macrophage responses.

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“…These genes are apparently repressed by CcpA without HPr-Ser-P. A similar number of genes are down-regulated (greater than twofold) in the ccpA mutant (IIb) and hence activated in L. monocytogenes by CcpA in the presence of glucose; these genes encode mainly metabolic enzymes. Interestingly inlA and inlB which, like the other PrfAdependent virulence genes, are up-regulated in the hprK mutant (see below) also belong to this set of genes, suggesting that expression of the inlAB operon which is under the control of several promoters, including a PrfA-dependent one (37,57), is also affected directly or indirectly by CcpA.…”

Section: Resultsmentioning

confidence: 99%

Interference of Components of the Phosphoenolpyruvate Phosphotransferase System with the Central Virulence Gene Regulator PrfA ofListeria monocytogenes

et al. 2007

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Analysis of Listeria monocytogenes ptsH, hprK, and ccpA mutants defective in carbon catabolite repression (CCR) control revealed significant alterations in the expression of PrfA-dependent genes. The hprK mutant showed high up-regulation of PrfA-dependent virulence genes upon growth in glucose-containing medium whereas expression of these genes was even slightly down-regulated in the ccpA mutant compared to the wild-type strain. The ptsH mutant could only grow in a rich culture medium, and here the PrfA-dependent genes were up-regulated as in the hprK mutant. As expected, HPr-Ser-P was not produced in the hprK and ptsH mutants and synthesized at a similar level in the ccpA mutant as in the wild-type strain. However, no direct correlation was found between the level of HPr-Ser-P or HPr-His-P and PrfA activity when L. monocytogenes was grown in minimal medium with different phosphotransferase system (PTS) carbohydrates. Comparison of the transcript profiles of the hprK and ccpA mutants with that of the wild-type strain indicates that the up-regulation of the PrfA-dependent virulence genes in the hprK mutant correlates with the down-regulation of genes known to be controlled by the efficiency of PTS-mediated glucose transport. Furthermore, growth in the presence of the non-PTS substrate glycerol results in high PrfA activity. These data suggest that it is not the component(s) of the CCR or the common PTS pathway but, rather, the component(s) of subsequent steps that seem to be involved in the modulation of PrfA activity.Listeria monocytogenes, a gram-positive, facultative intracellular human pathogen, escapes from the primary phagosome, replicates efficiently in the host cell's cytosol, and spreads from cell to cell. These processes, which are of major importance for pathogenesis of an L. monocytogenes infection, require several, well-characterized virulence factors (for recent reviews, see references 17, 32 and 63), like internalins (InlA, InlB, and

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Enhanced Synthesis of Internalin A inaroMutants ofListeria monocytogenesIndicates Posttranscriptional Control of theinlABmRNA

Cited by 39 publications

References 57 publications

Sigma B Contributes toListeria monocytogenesGastrointestinal Infection but Not to Systemic Spread in the Guinea Pig Infection Model

Sigma B Contributes toListeria monocytogenesGastrointestinal Infection but Not to Systemic Spread in the Guinea Pig Infection Model

Modulation of virulence factors in Francisella tularensis determines human macrophage responses

Interference of Components of the Phosphoenolpyruvate Phosphotransferase System with the Central Virulence Gene Regulator PrfA ofListeria monocytogenes

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