Repression of motility and flagellin production at 37 °C is stronger in<i>Listeria monocytogenes</i>than in the nonpathogenic species<i>Listeria innocua</i>

Kathariou, Sophia; Kanenaka, R.; Allen, Richard D.; Fok, Agnes K.; Mizumoto, C. Y.

doi:10.1139/m95-076

Cited by 32 publications

(22 citation statements)

References 6 publications

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“…At 25°C, L. monocytogenes is actively motile, with four to six peritrichous cells (40), and produces abundant flagellin (flaA encoded). In contrast, at 37°C, it is virtually nonmotile and produces little or no detectable flagellin (22). Here, we have identified two potential flagellar genes of L. monocytogenes: lmo0713, encoding a protein of 551 amino acids having 23% identity (and 45% similarity) with FliF of B. subtilis, the first structure to be assembled during flagellar biogenesis (23); and lmo0716, encoding a protein of 434 amino acids, having 43% amino acid identity (and 62% similarity) with FliI, an ATPase of B. subtilis that drives flagellar protein export.…”

Section: Resultsmentioning

confidence: 95%

“…At each condition tested, the ⌬fliF and ⌬fliI mutant strains exhibited a normal colony morphology on solid medium and a growth rate identical to that of the wild-type strain EGD-e in liquid medium (data not shown). The two mutants were assayed for mobility in semisolid BHI medium, as described by Kathariou and coworkers (22). The ability to swim is thought to be a ubiquitous behavioral trait exhibited by flagellated eubacteria.…”

Section: Resultsmentioning

confidence: 99%

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Role of FliF and FliI of Listeria monocytogenes in Flagellar Assembly and Pathogenicity

et al. 2005

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Flagellar structures have been shown to participate in virulence in a variety of intestinal pathogens. Here, we have identified two potential flagellar genes of Listeria monocytogenes: lmo0713, encoding a protein similar to the flagellar basal body component FliF, and lmo0716, encoding a protein similar to FliI, the cognate ATPase energizing the flagellar export apparatus. Expression of fliF and fliI appears to be downregulated at 37°C, like that of flaA, encoding flagellin. By constructing two chromosomal deletion mutants, we show that inactivation of either fliF or fliI (i) abolishes bacterial motility and flagella production, (ii) impairs adhesion and entry into nonphagocytic epithelial cells, and (iii) also reduces uptake by bone marrow-derived macrophages. However, the ⌬fliF and ⌬fliI mutations have only a minor impact on bacterial virulence in the mouse model, indicating that the flagellar secretion apparatus itself is not essential for survival in this animal model. Finally, among 100 human clinical isolates of L. monocytogenes tested, we found 20 strains still motile at 37°C. Notably, all these strains adhered less efficiently than strain EGD-e to Caco-2 cells at 37°C but showed no defect of intracellular multiplication. These data suggest that expression of the flagella at 37°C might hinder optimal adhesion to epithelial cells but has no impact on intracytosolic survival of L. monocytogenes.Listeria monocytogenes is a motile, facultative intracellular bacterium that causes food-borne infections in humans and animals, with symptoms of septicemia, meningitis, and meningo-encephalitis. This gram-positive bacterium is also widely distributed in the environment and is able to grow over a wide range of temperatures, pHs, and osmotic pressures (43). In animal models, bacteria have been shown to cross the gastrointestinal barrier and possibly penetrate the intestinal epithelial cells overlaying Peyer's patches (34,35). The organism then disseminates to the brain and to the spleen, liver, and other lymphatic systems (26). The virulence of L. monocytogenes is due to its capacity to invade and multiply within host cells, including macrophages and hepatocytes, as well as epithelial, endothelial, and neuronal cells. Each step of the infectious process is dependent on the production of virulence factors, including invasion proteins (InlA and InlB), listeriolysin O, phospholipases, and ActA, which are controlled by the pleiotropic transcriptional activator PrfA (11). The initial step of the internalization of L. monocytogenes into nonphagocytic cells involves an adhesion mediated in particular by internalin (InlA) and InlB surface proteins. InlA promotes entry of L. monocytogenes into human epithelial cells via E-cadherin as a receptor (30). InlB is involved in entry of the bacterium into a broad range of cell lines including hepatocytes and nonepithelial cells. InlB interacts with the receptor for the complement factor C1q, hepatocyte growth factor (c-Met), and glycosamine glycans (4). Recent findings suggest that ot...

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Section: Resultsmentioning

confidence: 95%

Section: Resultsmentioning

confidence: 99%

Role of FliF and FliI of Listeria monocytogenes in Flagellar Assembly and Pathogenicity

et al. 2005

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“…Swarming on soft agar was analyzed as described by Kathariou et al (30), with some modifications. Individual colonies were transferred to a petri plate containing tryptic soy broth (Difco) with 0.25% agar, and the motility plates were incubated for 24 h at 24 or 37°C.…”

Section: Methodsmentioning

confidence: 99%

“…This temperature regulation might serve as a mechanism to evade recognition by the innate immune system in the host. Interestingly, when comparing L. monocytogenes with the nonpathogenic but closely related species L. innocua, Kathariou et al (30) found that the repression of flagellin in L. innocua was not as strong as the repression in L. monocytogenes. The discrepancy of the in vivo virulence test of the ⌬flaA mutant with the in vitro invasion experiments with this mutant can be reconciled through the observation that the ⌬flaA mutant were present at lower levels than WT bacteria in TNFR-p55 Ϫ/Ϫ mice.…”

Section: Fig 6 Cfu After Ig Infection Of Tnfr-p55mentioning

confidence: 99%

Role of Flagellin and the Two-Component CheA/CheY System of Listeria monocytogenes in Host Cell Invasion and Virulence

Dons¹,

et al. 2004

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The flagellum protein flagellin of Listeria monocytogenes is encoded by the flaA gene. Immediately downstream of flaA, two genes, cheY and cheA, encoding products with homology to chemotaxis proteins of other bacteria, are located. In this study we constructed deletion mutants with mutations in flaA, cheY, and cheA to elucidate their role in the biology of infection with L. monocytogenes. The ⌬cheY, ⌬cheA, and double-mutant ⌬cheYA mutants, but not ⌬flaA mutant, were motile in liquid media. However, the ⌬cheA mutant had impaired swarming and the ⌬cheY and ⌬cheYA mutants were unable to swarm on soft agar plates, suggesting that cheY and cheA genes encode proteins involved in chemotaxis. The ⌬flaA, ⌬cheY, ⌬cheA, and ⌬cheYA mutants (grown at 24°C) showed reduced association with and invasion of Caco-2 cells compared to the wild-type strain. However, spleens from intragastrically infected BALB/c and C57BL/6 mice showed larger and similar numbers of the ⌬flaA and ⌬cheYA mutants, respectively, compared to the wild-type controls. Such a discrepancy could be explained by the fact that tumor necrosis factor receptor p55 deficient mice showed dramatically exacerbated susceptibility to the wild-type but unchanged or only slightly increased levels of the ⌬flaA or ⌬cheYA mutant. In summary, we show that listerial flaA, cheY, and cheA gene products facilitate the initial contact with epithelial cells and contribute to effective invasion but that flaA could also be involved in the triggering of immune responses.

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“…Bacterial swimming was investigated on swim plates as described elsewhere (Kathariou et al, 1995;Knudsen et al, 2004). Single colonies were inoculated in Tryptic Soy Broth (TSB) with 0.25 % agar and incubated at either 25 or 37 uC for 48 h.…”

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confidence: 99%

The DegU orphan response regulator of Listeria monocytogenes autorepresses its own synthesis and is required for bacterial motility, virulence and biofilm formation

et al. 2008

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The Gram-positive intracellular pathogen Listeria monocytogenes is endowed with 17 sets of genes encoding two-component systems. L. monocytogenes is closely related to the Grampositive model bacterium Bacillus subtilis, in which we have shown previously that the DegS/ DegU system plays a central role in controlling stationary phase adaptive responses, including degradative enzyme synthesis and competence. Although an orthologue of the DegU response regulator is present in L. monocytogenes, the gene encoding the cognate DegS kinase is conspicuously absent. We have inactivated the degU gene of L. monocytogenes and shown that DegU negatively regulates its own synthesis. Direct binding of L. monocytogenes DegU to its own promoter region was shown in vitro by gel mobility shift and DNase I footprinting experiments. DegU was also shown to bind upstream from the motB operon, which also encodes the GmaR anti-repressor of flagellar synthesis. In contrast to the situation in B. subtilis, DegU was shown to be essential for flagellar synthesis and bacterial motility in L. monocytogenes and is cotranscribed with the yviA gene located downstream. We also show that DegU is required for growth at high temperatures, adherence to plastic surfaces and the formation of efficient biofilms by L. monocytogenes. DegU plays a role in virulence of L. monocytogenes as well: in a murine intravenous infection model, an 11-fold increase in LD 50 was observed for the degU mutant. Taken together, our results indicate that despite the lack of the DegS kinase, DegU is fully functional as an orphan response regulator, and plays a central role in controlling several crucial adaptive responses in L. monocytogenes.

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Repression of motility and flagellin production at 37 °C is stronger inListeria monocytogenesthan in the nonpathogenic speciesListeria innocua

Cited by 32 publications

References 6 publications

Role of FliF and FliI of Listeria monocytogenes in Flagellar Assembly and Pathogenicity

Role of FliF and FliI of Listeria monocytogenes in Flagellar Assembly and Pathogenicity

Role of Flagellin and the Two-Component CheA/CheY System of Listeria monocytogenes in Host Cell Invasion and Virulence

The DegU orphan response regulator of Listeria monocytogenes autorepresses its own synthesis and is required for bacterial motility, virulence and biofilm formation

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