Penetration of Listeria monocytogenes into the host: A crucial step of the infectious process

Gaillard, Jean‐Louis; Berche, Patrick; Mounier, Joëlle; Richard, S.; Sansonetti, Philippe J.

doi:10.1016/0769-2609(87)90205-5

Cited by 35 publications

(30 citation statements)

References 15 publications

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“…4). One hour after gentamicin addition (i.e., Ϸ2 h after infection), by which time most intracellular Listeria have generally escaped from the phagocytic vacuole (25,26), fluorescence intensity was similar for the wt and the ⌬hpt mutant. This finding indicated that the two strains did not differ in phagosomal escape.…”

Section: Resultsmentioning

confidence: 99%

Hpt, a bacterial homolog of the microsomal glucose- 6-phosphate translocase, mediates rapid intracellular proliferation inListeria

Chico‐Calero

Suárez²,

González‐Zorn³

et al. 2001

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

234

192

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Efficient replication in vivo is essential for a microparasite to colonize its host and the understanding of the molecular mechanisms by which microbial pathogens grow within host tissues can lead to the discovery of novel therapies to treat infection. Here we present evidence that the foodborne bacterial pathogen Listeria monocytogenes, a facultative intracellular parasite, exploits hexose phosphates (HP) from the host cell as a source of carbon and energy to fuel fast intracellular growth. HP uptake is mediated by Hpt, a bacterial homolog of the mammalian translocase that transports glucose-6-phosphate from the cytosol into the endoplasmic reticulum in the final step of gluconeogenesis and glycogenolysis. Expression of the Hpt permease is tightly controlled by the central virulence regulator PrfA, which upon entry into host cells induces a set of virulence factors required for listerial intracellular parasitism. Loss of Hpt resulted in impaired listerial intracytosolic proliferation and attenuated virulence in mice. Hpt is the first virulence factor to be identified as specifically involved in the replication phase of a facultative intracellular pathogen. It is also a clear example of how adaptation to intracellular parasitism by microbial pathogens involves mimicry of physiological mechanisms of their eukaryotic host cells.

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Section: Resultsmentioning

confidence: 99%

Hpt, a bacterial homolog of the microsomal glucose- 6-phosphate translocase, mediates rapid intracellular proliferation inListeria

Chico‐Calero

Suárez²,

González‐Zorn³

et al. 2001

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

234

192

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“…Spontaneous mutant of BM410.5 (Leclercq et al, 1989) Spontaneous mutant of LO17 (Perez-Diaz et al, 1982) Spontaneous mutant of L. EGD (Gaillard et al, 1986) QB166 derivative (Courvalin & Carlier, 1986) Pasteur). Susceptibility tests were performed on BHI agar for the clinical isolates and on Mueller-Hinton agar for the other strains by the disk-agar diffusion test according to the recommendations of the Comite de I'Antibiogramme de la Societe Franqaise de Microbiologie (Courvalin & Soussy, 1996).…”

Section: Methodsmentioning

confidence: 99%

Conjugative transfer of tet(S) between strains of Enterococcus faecalis is associated with the exchange of large fragments of chromosomal DIMA

Francois¹,

Charles

Courvalin

1997

Microbiology

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The tetracycline resistance determinant tet(S) was first detected in antibiotic multiresistant Listeria monocytogenes BM4210 and subsequently in strains of Enterococcus faecalis. Transfer of tet(S) from clinical isolate E. faecalis BM4242 to E. faecalis strains JH2-2 and OGlRF was found to require the presence in the donor strain of the 55 kb conjugative plasmid plP825. Comparison of restriction endonuclease generated maps of the donor, the two recipients, and of four transconjugants indicated that transfer of tet(S) (i) was from chromosome to chromosome, (ii) resulted in the acquisition of an approximately 40 kb element in the same chromosomal region and (iii) was associated with the exchange of large chromosomal fragments. Similar observations were made following conjugal transfer of tet(S) from four other E. faecalis clinical isolates. ~~

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“…Cytochalasins, which have been shown to cause MF depolymerization (17), have been used to establish that S. typhi (and most other well-studied intracellular bacterial pathogens) use one or more MF-dependent pathways to enter epithelial cells (16,(18)(19)(20)(21). Although uptake of S. typhi Ty2 in the presence of 2 ,uM cytochalasin D was inhibited >99% into INT407 cells and >94% into bladder cells, cytochalasin-mediated effects were both strainand cell line-dependent for the Campylobacter and Citrobacter strains studied.…”

Section: Invasion Ability Of Selected Campylobacter and Citrobactermentioning

confidence: 99%

Unusual microtubule-dependent endocytosis mechanisms triggered by Campylobacter jejuni and Citrobacter freundii.

Oelschlaeger

Guerry

Kopecko

1993

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

270

291

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Bacterial invasion of six different human epithelial ceUl lines showed that some strains of the intestinal pathogen Campylobacterjejuni invaded intestinal cell lines at a level 102-104 times higher than reported previously for other Campylobacter strains. Separately, urinary tract isolates of Citrobacter freundii triggered a high-efficiency invasion of bladder cells. Use of multiple inhibitors with known effects on eukaryotic cell structures/processes allowed us to define in these genetically distinct bacterial genera unusual bacterial invasion mechanisms that uniquely require microtubules but not microfilaments. Campylobacterjejuni strain 81-176 uptake into 407 intestinal ceUls and Citrobacter entry into T24 bladder ceUls was blocked by microtubule depolymerization and inhibitors of coated-pit formation but not by microrflament depolymerization. Inhibitors of endosome acidification had no significant impact on intracellular survival of Campylobacterjejuni or Citrobacterfreundii, but monensin markedly reduced Citrobacter uptake. Epithelial cel invasion by both of these bacterial genera was dependent upon de novo bacterial protein synthesis but not upon de novo eukaryotic cel protein synthesis. In contrast to the T24 cel line-specific, strict microtubule-dependent uptake, Citrobacter entry into other cell lines was inhibited by both microtubule-and microfilament-depolymerization, suggesting that these bacteria encode two separate pathways for uptake (i, microtubule-dependent; ii, microfflament-dependent) that are cel line-specific and are recognized perhaps depending on the presence and abundance of appropriate eukaryotic receptors.

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Penetration of Listeria monocytogenes into the host: A crucial step of the infectious process

Cited by 35 publications

References 15 publications

Hpt, a bacterial homolog of the microsomal glucose- 6-phosphate translocase, mediates rapid intracellular proliferation inListeria

Hpt, a bacterial homolog of the microsomal glucose- 6-phosphate translocase, mediates rapid intracellular proliferation inListeria

Conjugative transfer of tet(S) between strains of Enterococcus faecalis is associated with the exchange of large fragments of chromosomal DIMA

Unusual microtubule-dependent endocytosis mechanisms triggered by Campylobacter jejuni and Citrobacter freundii.

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