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© Research
Publication : Cell host & microbe

Yersinia pseudotuberculosis effector YopJ subverts the Nod2/RICK/TAK1 pathway and activates caspase-1 to induce intestinal barrier dysfunction

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Cell host & microbe - 19 Apr 2012

Meinzer U, Barreau F, Esmiol-Welterlin S, Jung C, Villard C, Léger T, Ben-Mkaddem S, Berrebi D, Dussaillant M, Alnabhani Z, Roy M, Bonacorsi S, Wolf-Watz H, Perroy J, Ollendorff V, Hugot JP

Link to Pubmed [PMID] – 22520462

Cell Host Microbe 2012 Apr;11(4):337-51

Yersinia pseudotuberculosis is an enteropathogenic bacteria that disrupts the intestinal barrier and invades its host through gut-associated lymphoid tissue and Peyer’s patches (PP). We show that the Y. pseudotuberculosis effector YopJ induces intestinal barrier dysfunction by subverting signaling of the innate immune receptor Nod2, a phenotype that can be reversed by pretreating with the Nod2 ligand muramyl-dipeptide. YopJ, but not the catalytically inactive mutant YopJ(C172A), acetylates critical sites in the activation loops of the RICK and TAK1 kinases, which are central mediators of Nod2 signaling, and decreases the affinity of Nod2 for RICK. Concomitantly, Nod2 interacts with and activates caspase-1, resulting in increased levels of IL-1β. Finally, IL-1β within PP plays an essential role in inducing intestinal barrier dysfunction. Thus, YopJ alters intestinal permeability and promotes the dissemination of Yersinia as well as commensal bacteria by exploiting the mucosal inflammatory response.

https://www.ncbi.nlm.nih.gov/pubmed/22520462