InlA‐ but not InlB‐mediated internalization of <i>Listeria monocytogenes</i> by non‐phagocytic mammalian cells needs the support of other internalins

Bergmann, Birgit; Raffelsbauer, Diana; Kuhn, Michael; Goetz, Monika; Hom, Silke; Goebel, Werner

doi:10.1046/j.1365-2958.2002.02767.x

Cited by 80 publications

(69 citation statements)

References 49 publications

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“…For example, expression of the LPXTG-anchored InlJ by L. innocua leads to bacterial adhesion (but no invasion) to human JEG-3 and HT29 polarized epithelial cells , but its potential cell ligand has not been identified yet. The gene cluster inlGHE is required for full invasion of Caco-2 cells by the L. monocytogenes EGDe strain and it has been hypothesized that its expression may indirectly modulate the bacterial cell wall organization, therefore affecting InlA presentation at the L. monocytogenes surface (Bergmann et al 2002).…”

Section: Modulation Of Inla-and Inlb-dependent Invasion Pathways By Omentioning

confidence: 99%

Entry of Listeria monocytogenes in Mammalian Epithelial Cells: An Updated View

Pizarro‐Cerdá

Kühbacher

Cossart

2012

Cold Spring Harbor Perspectives in Medicine

226

203

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Listeria monocytogenes is a bacterial pathogen that promotes its internalization into host epithelial cells. Interaction between the bacterial surface molecules InlA and InlB and their cellular receptors E-cadherin and Met, respectively, triggers the recruitment of endocytic effectors, the subversion of the phosphoinositide metabolism, and the remodeling of the actin cytoskeleton that lead to bacterial engulfment. Additional bacterial surface and secreted virulence factors also contribute to entry, albeit to a lesser extent. Here we review the increasing number of signaling effectors that are reported as being subverted by L. monocytogenes during invasion of cultured cell lines. We also update the current knowledge of the early steps of in vivo cellular infection, which, as shown recently, challenges previous concepts generated from in vitro data.

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Section: Modulation Of Inla-and Inlb-dependent Invasion Pathways By Omentioning

confidence: 99%

Entry of Listeria monocytogenes in Mammalian Epithelial Cells: An Updated View

Pizarro‐Cerdá

Kühbacher

Cossart

2012

Cold Spring Harbor Perspectives in Medicine

226

203

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“…In contrast to InlA and InlB, none of these internalins seem to be able to induce phagocytosis by nonphagocytic mammalian cells (3). However, InlC may support InlA-mediated internalization into epithelial cells (3).…”

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confidence: 93%

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

2005

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Listeria monocytogenes mutants with deletions in aroA, aroB, or aroE exhibited strong posttranscriptional upregulation of internalin A (InlA) and InlB synthesis, which resulted in a more-than-10-fold increase in InlA-mediated internalization by epithelial Caco-2 cells and a 4-fold increase in InlB-mediated internalization by microvascular endothelial cells (human brain microvascular endothelial cells) compared to the wild-type strain. The increase in InlA and InlB production was not due to enhanced PrfA-and/or sigma factor B (SigB)-dependent inlAB transcription but was caused by enhanced translation of the inlAB transcripts in the aro mutants. All inlA(B) transcripts had a 396-nucleotide upstream 5 untranslated region (UTR). Different deletions introduced into this UTR led to significant reductions in InlA and InlB synthesis; enhanced translation of all of the truncated transcripts in the aro mutants was, however, still observed. Thus, translation of the inlAB transcripts was subject to two modes of posttranscriptional control, one mediated by the UTR structure and the other mediated by the aro mutation. The latter mode of control seemed to be related to the predominantly anaerobic metabolism of the aro mutants.

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“…The ability of bacteria with respect to adhesion to-, invasion of-, and intracellular growth within eukaryotic cells was assessed basically as described elsewhere (Bergmann et al, 2002;Rowan et al, 2000), with some minor modifications. Briefly, 2610 5 cells (1610 5 HBMEC cells) were seeded in 24-well tissue culture plates (VWR), grown for 48 h, and infected with 0.5 ml bacterial suspension (DispC mutant or wild-type strain) in MEM complete medium (for HBMEC, 25 mM HEPES and 1 mM sodium pyruvate was added to the medium) for 1 h at the desired m.o.i.…”

Section: Analysis Of Cell Surface Proteins By Ms and Western Blottingmentioning

confidence: 99%

A novel cell wall-anchored peptidoglycan hydrolase (autolysin), IspC, essential for Listeria monocytogenes virulence: genetic and proteomic analysis

Wang

Lin

2008

Microbiology

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InlA‐ but not InlB‐mediated internalization of Listeria monocytogenes by non‐phagocytic mammalian cells needs the support of other internalins

Cited by 80 publications

References 49 publications

Entry of Listeria monocytogenes in Mammalian Epithelial Cells: An Updated View

Entry of Listeria monocytogenes in Mammalian Epithelial Cells: An Updated View

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

A novel cell wall-anchored peptidoglycan hydrolase (autolysin), IspC, essential for Listeria monocytogenes virulence: genetic and proteomic analysis

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