Transcytosis of <i>Listeria monocytogenes</i> across the intestinal barrier upon specific targeting of goblet cell accessible E-cadherin

Nikitas, Georgios; Deschamps, Chantal; Disson, Olivier; Niault, Théodora; Cossart, Pascale; Lecuit, Marc

doi:10.1084/jem.20110560

Cited by 221 publications

(264 citation statements)

References 72 publications

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“…However, subsequent mechanisms to access the brain are likely to differ between host species. In humans, it is assumed that L. monocytogenes passes the gastrointestinal barrier and spreads haematogenously to the brain (Nikitas et al, 2011;Disson and Lecuit, 2012). In ruminants, there are indications that the pathogen enters the cranial nerves via the oral epithelium or conjunctivae (Charlton and Garcia, 1977).…”

Section: Pathogenesis Of Cns Infectionmentioning

confidence: 99%

Listeria monocytogenes infection in ruminants: Is there a link to the environment, food and human health? A review

Walland¹,

Lauper²,

Frey³

et al. 2015

SAT

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Listeria (L.) monocytogenes is widely distributed in the environment, but also has the ability to cause serious invasive disease in ruminants and humans. This review provides an overview of listeriosis in ruminants and discusses our insufficient understanding of reservoirs and possible cycling ofL. monocytogenes between animal and human hosts, food and the environment. It indicates gaps in our knowledge of the role of genetic subtypes in L. monocytogenes ecology and virulence as well as risk factors, in vivo diagnostics and pathogenesis of listeriosis in ruminants. Filling these gaps will contribute to improving the control of L. monocytogenes and enhancing disease prevention. As the prevalence of listeriosis in ruminants in Switzerland is likely to be underestimated, propositions concerning improvement options for surveillance of listeriosis in ruminants are provided. Summary Listeria (L.) monocytogenes is widely distributed in the environment, but also has the ability to cause serious invasive disease in ruminants and humans. This review provides an overview of listeriosis in ruminants and discusses our insufficient understanding of reservoirs and possible cycling of L. monocytogenes between animal and human hosts, food and the environment. It indicates gaps in our knowledge of the role of genetic subtypes in L. monocytogenes ecology and virulence as well as risk factors, in vivo diagnostics and pathogenesis of listeriosis in ruminants. Filling these gaps will contribute to improving the control of L. monocytogenes and enhancing disease prevention. As the prevalence of listeriosis in ruminants in Switzerland is likely to be underestimated, propositions concerning improvement options for surveillance of listeriosis in ruminants are provided.

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Section: Pathogenesis Of Cns Infectionmentioning

confidence: 99%

Listeria monocytogenes infection in ruminants: Is there a link to the environment, food and human health? A review

Walland¹,

Lauper²,

Frey³

et al. 2015

SAT

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“…It has now been shown that E-cadherin is luminally accessible not only around extruding enterocytes at the tip and lateral sides of villi, but also particularly around mucus-expelling goblet cells (GCs) and in villus epithelial folds. L. monocytogenes preferentially adheres to accessible E-cadherin on GCs in a ligated loop of transgenic mice expressing human E-cadherin, is internalized, rapidly transcytosed across the intestinal epithelium, and released in the lamina propria by exocytosis from where it disseminates systemically (Nikitas et al 2011). L. monocytogenes is thus able to exploit intrinsic tissue heterogeneity to access its receptor.…”

Section: Translocation Across Enterocytesmentioning

confidence: 99%

Concepts and Mechanisms: Crossing Host Barriers

Doran

Banerjee

Disson

et al. 2013

Cold Spring Harbor Perspectives in Medicine

113

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“…These observations suggest that, at the intestinal level, Lm takes advantage of adherens junction reorganization to target acc-Ecad in an InlA-dependent manner and to be internalized without the need for additional activation of PI3-K signaling, thus making it independent of InlB. similar to ECs and EEFs, mucus expelling-GCs undergo extensive shape changes accompanied by cell-cell junction reorganization (Hull and Staehelin, 1976;Porvaznik et al, 1983;Nikitas et al, 2011). Moreover, epithelial cell differentiation in GCs also involves PI3-K signaling cascade (Durual et al, This observation further challenges the relevance of using InlA m -expressing Lm to study host intestinal barrier crossing.…”

Section: Discussionmentioning

confidence: 93%

“…InlA is necessary and sufficient to mediate the crossing of the intestinal barrier by targeting luminally accessible Ecad (acc-Ecad), in particular on mucus-secreting goblet cells (GCs; Lecuit et al, 2001;Nikitas et al, 2011), whereas InlB is not involved in this process (Khelef et al, 2006). In contrast, in third-trimester and term placentas, the crossing of the trophoblastic barrier requires the conjugated action of InlA and InlB Disson et al, 2008), and Lm invades the syncytiotrophoblasts that express Ecad accessible to mother blood-borne bacteria .…”

Section: Lm Intestinal Target Cells Exhibit a Higher Intrinsic Akt Phmentioning

confidence: 99%

“…(A, C, D, E, and F) Immunoblots were performed at least two times. Densitometry was performed and the ratio of P-Akt over total Akt is relative to the PBS, for which the value is normalized to 1. the crossing of the placental barrier (Lecuit et al, 2001;Khelef et al, 2006;Disson et al, 2008;Nikitas et al, 2011), where almost no P-Akt is detected. The same holds true in human placenta, where InlB is necessary to invade the trophoblast in ex vivo term placental villous explants.…”

Section: Inlb Is Not Involved In Lm Crossing Of the Intestinal Barriermentioning

confidence: 99%

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

Gessain¹,

Tsai²,

Travier³

et al. 2015

J Cell Biol

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Invasion of nonphagocytic cells, a critical property of Listeria monocytogenes (Lm) that enables it to cross host barriers, is mediated by the interaction of two bacterial surface proteins, InlA and InlB, with their respective receptors E-cadherin and c-Met. AlthoughInlA-E-cadherin interaction is necessary and sufficient for Lm crossing of the intestinal barrier, both InlA and InlB are required for Lm crossing of the placental barrier. The mechanisms underlying these differences are unknown. Phosphoinositide 3-kinase (PI3-K) is involved in both InlA-and InlB-dependent pathways. Indeed, InlA-dependent entry requires PI3-K activity but does not activate it, whereas InlB-c-Met interaction activates PI3-K. We show that Lm intestinal target cells exhibit a constitutive PI3-K activity, rendering InlB dispensable for InlA-dependent Lm intestinal barrier crossing. In contrast, the placental barrier does not exhibit constitutive PI3-K activity, making InlB necessary for InlA-dependent Lm placental invasion. Here, we provide the molecular explanation for the respective contributions of InlA and InlB to Lm host barrier invasion, and reveal the critical role of InlB in rendering cells permissive to InlA-mediated invasion. This study shows that PI3-K activity is critical to host barrier permissiveness to microbes, and that pathogens exploit both similarities and differences of host barriers to disseminate.

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Transcytosis of Listeria monocytogenes across the intestinal barrier upon specific targeting of goblet cell accessible E-cadherin

Abstract: Listeria monocytogenes targets accessible E-cadherin expressed on mucus-producing goblet cells to invade the intestinal tissue.

Cited by 221 publications

References 72 publications

Listeria monocytogenes infection in ruminants: Is there a link to the environment, food and human health? A review

Listeria monocytogenes infection in ruminants: Is there a link to the environment, food and human health? A review

Concepts and Mechanisms: Crossing Host Barriers

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

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