Listeria monocytogenes and listeric infections.

Gray, M L; Killinger, A H

doi:10.1128/mmbr.30.2.309-382.1966

Cited by 530 publications

(335 citation statements)

References 42 publications

(126 reference statements)

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“…This Gram-positive bacterium, which widely spreads in nature, is a facultative intracellular pathogen capable to invade and grow in most host cells, including macrophages (Mackaness, 1962;Vazquez-Boland et al ., 2001) and bone marrow myeloid precursors differentiated to monocytes in vitro (Kolb-Maurer et al ., 2002). It is responsible for sporadic severe infections in humans and most animal species, which are characterized by a systemic dissemination, mainly resulting in maternofetal infections and meningoencephalitis (Gray and Killinger, 1966). These features can be easily reproduced during experimental infection (Prats et al ., 1992;Berche, 1995;Lopez et al ., 1999;Bakardjiev et al ., 2004).…”

Section: Introductionmentioning

confidence: 99%

Listeria monocytogenes-infected bone marrow myeloid cells promote bacterial invasion of the central nervous system

Join‐Lambert

Ezine

Monnier

et al. 2004

Cellular Microbiology

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Section: Introductionmentioning

confidence: 99%

Listeria monocytogenes-infected bone marrow myeloid cells promote bacterial invasion of the central nervous system

Join‐Lambert

Ezine

Monnier

et al. 2004

Cellular Microbiology

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“…Listeria monocytogenes is a Gram-positive facultative intracellular bacterial pathogen that can cause serious food-borne infections in neonates, elderly people, pregnant women and immunocompromised individuals. The mortality rate for listeriosis is high and results from clinical manifestations such as meningitis, septicaemia, and, in pregnant women, abortion of the fetus (Gray and Killinger, 1966;Gellin and Broome, 1989;Lorber, 1997). L. monocytogenes is able to invade, replicate and spread from cell to cell within a wide variety of cell types (reviewed by Sheehan et al ., 1994;Kreft and Vazquez-Boland, 2001;Vazquez-Boland et al ., 2001).…”

Section: Introductionmentioning

confidence: 99%

Evidence implicating the 5′ untranslated region ofListeria monocytogenes actAin the regulation of bacterial actin-based motility

Wong

Bouwer

Freitag

2004

Cellular Microbiology

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SummaryThe ActA protein of Listeria monocytogenes is a major virulence factor, essential for the recruitment and polymerization of host actin filaments that lead to intracellular motility and cell-to-cell spread of bacteria within the infected host. The expression of actA is tightly regulated and is strongly induced only when L. monocytogenes is within the host cytosol. Intracellular induction of actA expression is mediated through a single promoter element that directs the expression of a messenger RNA with a long (150 bp) 5 ′ ′ ′ ′ untranslated region (UTR). Deletion of the actA +3 to +130 upstream region was found to result in bacterial mutants that were no longer capable of intracellular actin recruitment or cell-to-cell spread, thus indicating that this region is important for actA expression. L. monocytogenes strains that contained smaller deletions (21-23 bp) within the actA upstream region demonstrated a range of actA expression levels that coincided with the amount of bacterial cell-tocell spread observed within infected monolayers. A correlation appeared to exist between levels of actA expression and the ability of L. monocytogenes to transition from uniform actin accumulation surrounding individual bacteria (actin clouds) to directional assembly and the formation of actin tails. Bacterial mutants containing deletions that most significantly altered the predicted secondary structure of the actA mRNA 5 ′ ′ ′ ′ UTR had the largest reductions in actA expression. These results suggest that the actA 5 ′ ′ ′ ′ UTR is required for maximal ActA synthesis and that a threshold level of ActA synthesis must be achieved to promote the transition from bacteria-associated actin clouds to directional actin assembly and movement.

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“…The Gram positive bacterium responsible for human listeriosis, Listeria monocytogenes, was first isolated from rabbits that became ill during a laboratory epidemic in 1926 [Murray et al, 19261. Since then, the organism has been found in many wild and domestic mammals and birds and has been isolated from soil, water, sewage, and other environmental sources [Bortolussi et al, 19851. Although various modes of entry have been described, human infections usually follow transplacental [Gray and Killinger, 19661 or transintestinal [Stamm et al, 19821 routes. L. monocytogenes is also a veterinary pathogen associated with spontaneous abortion and 0 1994 Wiley-Liss, Inc. encephalitis in sheep and cattle [Gray and Killinger, 1966; Bortolussi et a]., 19851.…”

Section: Introductionmentioning

confidence: 99%

Dynamics of actin and alpha‐actinin in the tails of Listeria monocytogenes in Infected PtK₂ Cells

Nanavati

Ashton

Sanger

et al. 1994

Cell Motil. Cytoskeleton

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Listeria monocytogenes can penetrate and multiply within a variety of cell types, including the PtK2 kidney epithelial line. Once released within the cytoplasm, L. monocytogenes acquires the capacity for rapid movement through the host cell [Dabiri et al., 1990: Proc. Natl. Acad. Sci. 87:6068-6072]. In the process, actin monomers are inserted in proximity to one end of the bacterium, forming a column or tail of actin filaments [Sanger et al., 1992: Infect. Immun. 60:3609-3619]. The rate of new actin filament growth correlates closely with the speed of bacterial migration. In this study we have used fluorescently labeled actin and alpha-actinin to monitor the movement and turnover rate of actin and alpha-actinin molecules in the tails. The half-lives of the actin and alpha-actinin present in the tails are approximately the same: actin, 58.7 sec; alpha-actinin, 55.3 sec. The half-life of alpha-actinin surrounding a dividing bacterium was 30 sec, whereas its half-life in the tails that formed behind the two daughter cells was about 20-30% longer. We discovered that the speeds of the bacteria are not constant, but show aperiodic episodes of decreased and increased speeds. There is a fluctuation also in the intensities of the fluorescent probes at the bacterium/tail interface, implying that there is a fluctuation in the number of actin filaments forming there. There was no strong correlation, however, between these fluctuating intensities and changes in speed of the bacteria. These measurements suggest that while actin polymerization at the bacterial surface is coupled to the movement of the bacterium, the periodic changes in intracellular motility are not a simple function of the number of actin filaments nucleating at the bacterial surfaces.

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Listeria monocytogenes and listeric infections.

Cited by 530 publications

References 42 publications

Listeria monocytogenes-infected bone marrow myeloid cells promote bacterial invasion of the central nervous system

Listeria monocytogenes-infected bone marrow myeloid cells promote bacterial invasion of the central nervous system

Evidence implicating the 5′ untranslated region ofListeria monocytogenes actAin the regulation of bacterial actin-based motility

Dynamics of actin and alpha‐actinin in the tails of Listeria monocytogenes in Infected PtK₂ Cells

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Listeria monocytogenes and listeric infections.

Cited by 530 publications

References 42 publications

Listeria monocytogenes-infected bone marrow myeloid cells promote bacterial invasion of the central nervous system

Listeria monocytogenes-infected bone marrow myeloid cells promote bacterial invasion of the central nervous system

Evidence implicating the 5′ untranslated region ofListeria monocytogenes actAin the regulation of bacterial actin-based motility

Dynamics of actin and alpha‐actinin in the tails of Listeria monocytogenes in Infected PtK2 Cells

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Dynamics of actin and alpha‐actinin in the tails of Listeria monocytogenes in Infected PtK₂ Cells