PI3-kinase activation is critical for host barrier permissiveness to <i>Listeria monocytogenes</i>

Gessain, Grégoire; Tsai, Yu Huan; Travier, Laetitia; Bonazzi, Matteo; Grayo, Solène; Cossart, Pascale; Charlier, Caroline; Disson, Olivier; Lecuit, Marc

doi:10.1084/jem.20141406

Cited by 63 publications

(38 citation statements)

References 59 publications

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“…Furthermore, mice infected with the Δ mouR + mouR complemented strain showed bacterial levels comparable to the WT, revealing a restored phenotype (Figure 7C ). Lm was previously shown to preferentially invade intestinal Peyer's patches following oral inoculation in the mouse model used in our study ( 73 , 74 ). We thus assessed numbers of Lm present in mouse Peyer's patches 72 h after oral inoculation.…”

Section: Resultsmentioning

confidence: 59%

MouR controls the expression of the Listeria monocytogenes Agr system and mediates virulence

Pinheiro

Lisboa

Pombinho

et al. 2018

Nucleic Acids Research

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The foodborne pathogen Listeria monocytogenes (Lm) causes invasive infection in susceptible animals and humans. To survive and proliferate within hosts, this facultative intracellular pathogen tightly coordinates the expression of a complex regulatory network that controls the expression of virulence factors. Here, we identified and characterized MouR, a novel virulence regulator of Lm. Through RNA-seq transcriptomic analysis, we determined the MouR regulon and demonstrated how MouR positively controls the expression of the Agr quorum sensing system (agrBDCA) of Lm. The MouR three-dimensional structure revealed a dimeric DNA-binding transcription factor belonging to the VanR class of the GntR superfamily of regulatory proteins. We also showed that by directly binding to the agr promoter region, MouR ultimately modulates chitinase activity and biofilm formation. Importantly, we demonstrated by in vitro cell invasion assays and in vivo mice infections the role of MouR in Lm virulence.

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Section: Resultsmentioning

confidence: 59%

MouR controls the expression of the Listeria monocytogenes Agr system and mediates virulence

Pinheiro

Lisboa

Pombinho

et al. 2018

Nucleic Acids Research

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“…In contrast, the placental barrier does not exhibit constitutive PI3-K activity, rendering InlB necessary for InlA-dependent Lm placental invasion. These results provide a molecular explanation for the respective contributions of InlA and InlB to Lm host barriers' invasion, and reveal the critical role of InlB in rendering cells permissive to InlAmediated invasion (Gessain et al, 2015). They also show that PI3-K activity is critical to host barriers' permissiveness to microbes, and that pathogens exploit both similarities and differences of host barriers to disseminate.…”

Section: Listeria Monocytogenes Crossing Of the Placental Barriermentioning

confidence: 60%

Listeria monocytogenes, a model in infection biology

Lecuit

2020

Cellular Microbiology

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Listeria monocytogenes causes listeriosis, a systemic infection which manifests as bacteremia, often complicated by meningoencephalitis in immunocompromised individuals and the elderly, and fetal‐placental infection in pregnant women. It has emerged over the past decades as a major foodborne pathogen, responsible for numerous outbreaks in Western countries, and more recently in Africa. L. monocytogenes' pathogenic properties have been studied in detail, thanks to concomitant advances in biological sciences, in particular molecular biology, cell biology and immunology. L. monocytogenes has also been instrumental to basic advances in life sciences. L. monocytogenes therefore stands both a tool to understand biology and a model in infection biology. This review briefly summarises the clinical and some of the pathophysiological features of listeriosis. In the context of this special issue, it highlights some of the major discoveries made by Pascale Cossart in the fields of molecular and cellular microbiology since the mid‐eighties regarding the identification and characterisation of multiple bacterial and host factors critical to L. monocytogenes pathogenicity. It also briefly summarises some of the key findings from our laboratory on this topic over the past years.

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“…Western blots of phosphotyrosine enriched protein fractions showed decreased levels of the PI3K p85 subunit in K8/K18-depleted cells (Figure 4C ), indicating an impaired association of PI3K with tyrosine phosphorylated proteins in absence of keratins and suggesting a defect in PI3K activation. In addition, K18-depleted cell lysates were directly subjected to immunoblot analysis to detect phosphorylation of Akt on serine 473 (P-Akt, S473), a direct downstream target of PI3K activity (Basar et al, 2005 ; Vanhaesebroeck et al, 2012 ; Gessain et al, 2015 ). As expected, in control cells HGF stimulation induced robust phosphorylation of Akt, which is extensively compromised in K18-depleted cells (Figures 4D,E ).…”

Section: Resultsmentioning

confidence: 99%

Epithelial Keratins Modulate cMet Expression and Signaling and Promote InlB-Mediated Listeria monocytogenes Infection of HeLa Cells

Cruz

Pereira-Castro

Almeida

et al. 2018

Front. Cell. Infect. Microbiol.

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The host cytoskeleton is a major target for bacterial pathogens during infection. In particular, pathogens usurp the actin cytoskeleton function to strongly adhere to the host cell surface, to induce plasma membrane remodeling allowing invasion and to spread from cell to cell and disseminate to the whole organism. Keratins are cytoskeletal proteins that are the major components of intermediate filaments in epithelial cells however, their role in bacterial infection has been disregarded. Here we investigate the role of the major epithelial keratins, keratins 8 and 18 (K8 and K18), in the cellular infection by Listeria monocytogenes. We found that K8 and K18 are required for successful InlB/cMet-dependent L. monocytogenes infection, but are dispensable for InlA/E-cadherin-mediated invasion. Both K8 and K18 accumulate at InlB-mediated internalization sites following actin recruitment and modulate actin dynamics at those sites. We also reveal the key role of K8 and K18 in HGF-induced signaling which occurs downstream the activation of cMet. Strikingly, we show here that K18, and at a less extent K8, controls the expression of cMet and other surface receptors such TfR and integrin β1, by promoting the stability of their corresponding transcripts. Together, our results reveal novel functions for major epithelial keratins in the modulation of actin dynamics at the bacterial entry sites and in the control of surface receptors mRNA stability and expression.

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PI3-kinase activation is critical for host barrier permissiveness to Listeria monocytogenes

Cited by 63 publications

References 59 publications

MouR controls the expression of the Listeria monocytogenes Agr system and mediates virulence

MouR controls the expression of the Listeria monocytogenes Agr system and mediates virulence

Listeria monocytogenes, a model in infection biology

Epithelial Keratins Modulate cMet Expression and Signaling and Promote InlB-Mediated Listeria monocytogenes Infection of HeLa Cells

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