Glucose and glucose 6-phosphate as carbon sources in extra- and intracellular growth of enteroinvasive Escherichia coli and Salmonella enterica

Götz, Andreas W.; Goebel, Werner

doi:10.1099/mic.0.034744-0

Cited by 41 publications

(50 citation statements)

References 38 publications

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“…Carbohydrate metabolism has also been implicated in pathogenesis of enteroinvasive E. coli (EIEC), which is closely related to Shigella. In a cell culture model, an EIEC mutant defective in both glucose and mannose transport was significantly impaired in adherence and invasion (15). The intracellular pathogen Listeria monocytogenes appears to maximize its ability to grow intracellularly by using multiple carbon sources, such as glucose-6-phosphate and glycerol (26,27).…”

Section: Discussionmentioning

confidence: 99%

CsrA and Cra Influence Shigella flexneri Pathogenesis

Gore

Payne

2010

Infect Immun

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Shigella flexneri is a facultative intracellular pathogen that invades and disrupts the colonic epithelium. In order to thrive in the host, S. flexneri must adapt to environmental conditions in the gut and within the eukaryotic cytosol, including variability in the available carbon sources and other nutrients. We examined the roles of the carbon consumption regulators CsrA and Cra in a cell culture model of S. flexneri virulence. CsrA is an activator of glycolysis and a repressor of gluconeogenesis, and a csrA mutant had decreased attachment and invasion of cultured cells. Conversely, Cra represses glycolysis and activates gluconeogenesis, and the cra mutant had an increase in both attachment and invasion compared to the wild-type strain. Both mutants were defective in plaque formation. The importance of the glycolytic pathway in invasion and plaque formation was confirmed by testing the effect of a mutation in the glycolysis gene pfkA. The pfkA mutant was noninvasive and had cell surface alterations as indicated by decreased sensitivity to SDS and an altered lipopolysaccharide profile. The loss of invasion by the csrA and pfkA mutants was due to decreased expression of the S. flexneri virulence factor regulators virF and virB, resulting in decreased production of Shigella invasion plasmid antigens (Ipa). These data indicate that regulation of carbon metabolism and expression of the glycolysis gene pfkA are critical for synthesis of the virulence gene regulators VirF and VirB, and both the glycolytic and gluconeogenic pathways influence steps in S. flexneri invasion and plaque formation.The Gram-negative bacterium Shigella flexneri is a causative agent of shigellosis, a severe infection of the colonic epithelium. S. flexneri is primarily transmitted between hosts via the fecal-oral route to its infective site in the colon. Following attachment to colonic epithelial cells, S. flexneri induces its own uptake and replicates in the host cell cytosol. The bacterium then spreads directly to adjacent epithelial cells, thereby propagating itself within the intestinal epithelium (24). S. flexneri invasion requires genes on the 220-kb virulence plasmid (50, 51). These include the Ipa effectors necessary for bacterial entry into colonic epithelial cells (32) and the type III secretion system that delivers the effectors to the host cytosol (3,33,34,65).

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Section: Discussionmentioning

confidence: 99%

CsrA and Cra Influence Shigella flexneri Pathogenesis

Gore

Payne

2010

Infect Immun

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“…Carbohydrate phosphotransferase systems were encoded by the genes ptsG/crr, manXYZ, fruBA, malX/crr, scrA/crr, and bglF, and glucose 6-phosphate was taken up by both pathogens via the UhpT transporter, which is under the control of a complex two-component system (uhpABC). S. Typhimurium mutants defective for the uptake of glucose and mannose (⌬ptsG manXYZ) and glucose 6-phosphate (⌬uhpT) have less capability for intracellular replication in undifferentiated Caco-2 cells, and the ⌬ptsG manXYZ uhpT triple mutant is still able to replicate within the vacuoles (398).…”

Section: Cell Interaction Cell Entry and Intracellular Lifestylementioning

confidence: 99%

“…EIEC strains growing in the cytosol of undifferentiated confluent Caco-2 cells utilize glucose, but not glucose 6-phosphate, or other phosphorylated carbohydrates, gluconate, or fatty acids as their main carbon substrates (397,398) (Table 2). Moreno et al (440) have compared the intracellular lifestyle of EIEC within fully differentiated Caco-2 cells at the cellular and molecular levels to that of S. flexneri.…”

Section: Cell Interaction Cell Entry and Intracellular Lifestylementioning

confidence: 99%

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Moal

Servin

2013

Microbiol Mol Biol Rev

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SUMMARY Hosts are protected from attack by potentially harmful enteric microorganisms, viruses, and parasites by the polarized fully differentiated epithelial cells that make up the epithelium, providing a physical and functional barrier. Enterovirulent bacteria interact with the epithelial polarized cells lining the intestinal barrier, and some invade the cells. A better understanding of the cross talk between enterovirulent bacteria and the polarized intestinal cells has resulted in the identification of essential enterovirulent bacterial structures and virulence gene products playing pivotal roles in pathogenesis. Cultured animal cell lines and cultured human nonintestinal, undifferentiated epithelial cells have been extensively used for understanding the mechanisms by which some human enterovirulent bacteria induce intestinal disorders. Human colon carcinoma cell lines which are able to express in culture the functional and structural characteristics of mature enterocytes and goblet cells have been established, mimicking structurally and functionally an intestinal epithelial barrier. Moreover, Caco-2-derived M-like cells have been established, mimicking the bacterial capture property of M cells of Peyer's patches. This review intends to analyze the cellular and molecular mechanisms of pathogenesis of human enterovirulent bacteria observed in infected cultured human colon carcinoma enterocyte-like HT-29 subpopulations, enterocyte-like Caco-2 and clone cells, the colonic T84 cell line, HT-29 mucus-secreting cell subpopulations, and Caco-2-derived M-like cells, including cell association, cell entry, intracellular lifestyle, structural lesions at the brush border, functional lesions in enterocytes and goblet cells, functional and structural lesions at the junctional domain, and host cellular defense responses.

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“…However, at this stage of the work, we cannot totally exclude the possibility that exSPs would directly enter the cell via specific transporters similar to the uhp system (Götz and Göbel 2010) and controlled by PhoP. This hypothesis seems unlikely since a genomic scale analysis of possible carbohydrate transporters (Bertram et al 2004) did not identified, in S. coelicolor, an uhp-like uptake system.…”

Section: Discussionmentioning

confidence: 89%

“…The utilization of sugar phosphates is PhoPdependent Theoretically, exSPs could be up-taken as such by a specific transporter similar to the uhp (uptake of hexose phosphate) system of enteroenvasive Escherichia coli and Salmonella enterica (Götz and Göbel 2010).…”

Section: Effect Of Extracellular Sugar-phosphates On Streptomyces Devmentioning

confidence: 99%

Extracellular sugar phosphates are assimilated by Streptomyces in a PhoP-dependent manner

Tenconi

Jourdan

Motté

et al. 2012

Antonie van Leeuwenhoek

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Filamentous microorganisms of the bacterial genus Streptomyces have a complex life cycle that includes physiological and morphological differentiations. It is now fairly well accepted that lysis of Streptomyces vegetative mycelium induced by programmed cell death (PCD) provides the required nutritive sources for the bacterium to erect sporeforming aerial hyphae. However, little is known regarding cellular compounds released during PCD and the contribution of these molecules to the feeding of surviving cells in order to allow them to reach the late stages of the developmental program. In this work we assessed the effect of extracellular sugar phosphates (that are likely to be released in the environment upon cell lysis) on the differentiation processes.We demonstrated that the supply of phosphorylated sugars, under inorganic phosphate limitation, delays the occurrence of the second round of PCD, blocks streptomycetes life cycle at the vegetative state and inhibits antibiotic production. The mechanism by which sugar phosphates affect development was shown to involve genes of the Pho regulon that are under the positive control of the two component system PhoR/PhoP. Indeed, the inactivation of the response regulator phoP of Streptomyces lividans prevented the 'sugar phosphate effect' whereas the S. lividans ppk (polyphosphate kinase) deletion mutant, known to overexpress the Pho regulon, presented an enhanced response to phosphorylated sugars.

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Glucose and glucose 6-phosphate as carbon sources in extra- and intracellular growth of enteroinvasive Escherichia coli and Salmonella enterica

Cited by 41 publications

References 38 publications

CsrA and Cra Influence Shigella flexneri Pathogenesis

CsrA and Cra Influence Shigella flexneri Pathogenesis

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Extracellular sugar phosphates are assimilated by Streptomyces in a PhoP-dependent manner

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