Listerial invasion protein internalin B promotes entry into ileal Peyer's patches in vivo

Chiba, Sayuri; Nagai, Takeshi; Hayashi, Toshiyuki; Baba, Yukiko; Nagai, Shigenori; Koyasu, Shigeo

doi:10.1111/j.1348-0421.2010.00292.x

Cited by 51 publications

(47 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, in KIE16P mice, we did not observe any role for InlB at Peyer's patch level. This suggests that, in models permissive to both InlA and InlB, InlB-requirement for Lm invasion of Peyer's patch There are apparently conflicting data regarding the role of InlB in the crossing of intestinal barrier: whereas we have repeatedly found no role for InlB in Lm crossing of the intestinal barrier in in vivo models permissive to both InlA-Ecad and InlB-c-Met interactions (Khelef et al, 2006;Disson et al, 2008), it has been reported by others that InlB accelerates invasion at villous tips in an experimental model using murinized InlA (Pentecost et al, 2010) and plays a role at the Peyer's patch level in WT mice (Chiba et al, 2011). Here, we have confirmed these results and revisited their interpretations in light of our new investigations: we compared the infection of murinized InlA (InlA m ) expressing Lm (Wollert et al, 2007) in WT mice (Pentecost et al, 2010) and the infection of WT Lm in KIE16P mice expressing humanized mEcad (Disson et al, 2008) at the villous tip level.…”

Section: Discussioncontrasting

confidence: 54%

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

Gessain¹,

Tsai²,

Travier³

et al. 2015

J Cell Biol

View full text Add to dashboard Cite

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.

show abstract

Section: Discussioncontrasting

confidence: 54%

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

Gessain¹,

Tsai²,

Travier³

et al. 2015

J Cell Biol

View full text Add to dashboard Cite

show abstract

“…The region from amino acid residues 184 -200 showed homology to leucine-rich repeats of internalin B protein of Listeria monocytogenes. The leucine-rich repeats of internalin B has been shown to be required for inducing phagocytosis in non-phagocytic cells such as hepatocytes and endothelial and epithelial cells (46,47). We reported that FTL_0325 suppresses proinflammatory cytokines primarily by interfering with NF-B signaling (37).…”

Section: Discussionmentioning

confidence: 90%

Repression of Inflammasome by Francisella tularensis during Early Stages of Infection

Dotson

Rabadi

Westcott

et al. 2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Entry through ileal Peyer's patches via M cells does not rely on InlA. It has been reported to require Listeria invasion protein InlB (Chiba et al, 2011). After translocation, bacteria reach lymph nodes, the liver and spleen and finally secondary target sites of infection, including the central nervous system and the placenta.…”

Section: Introductionmentioning

confidence: 99%

The bacterial pathogen Listeria monocytogenes and the interferon family: type I, type II and type III interferons

Dussurget

Bierne

Cossart

2014

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

Interferons (IFNs) are secreted proteins of the cytokine family that regulate innate and adaptive immune responses to infection. Although the importance of IFNs in the antiviral response has long been appreciated, their role in bacterial infections is more complex and is currently a major focus of investigation. This review summarizes our current knowledge of the role of these cytokines in host defense against the bacterial pathogen Listeria monocytogenes and highlights recent discoveries on the molecular mechanisms evolved by this intracellular bacterium to subvert IFN responses.

show abstract

Listerial invasion protein internalin B promotes entry into ileal Peyer's patches in vivo

Cited by 51 publications

References 22 publications

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

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

Repression of Inflammasome by Francisella tularensis during Early Stages of Infection

The bacterial pathogen Listeria monocytogenes and the interferon family: type I, type II and type III interferons

Contact Info

Product

Resources

About