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© Christine Schmitt, Meriem El Ghachi, Jean-Marc Panaud
Bactérie Helicobacter pylori en microscopie électronique à balayage. Agent causal de pathologies de l'estomac : elle est responsable des gastrites chroniques, d'ulcères gastriques et duodénaux et elle joue un rôle important dans la genèse des cancers gastriques (adénocarcinomes et lymphomes).
Publication : Cell host & microbe

The immune receptor NOD1 and kinase RIP2 interact with bacterial peptidoglycan on early endosomes to promote autophagy and inflammatory signaling

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Cell host & microbe - 17 Apr 2014

Irving AT, Mimuro H, Kufer TA, Lo C, Wheeler R, Turner LJ, Thomas BJ, Malosse C, Gantier MP, Casillas LN, Votta BJ, Bertin J, Boneca IG, Sasakawa C, Philpott DJ, Ferrero RL, Kaparakis-Liaskos M

Link to Pubmed [PMID] – 24746552

Cell Host Microbe 2014 May;15(5):623-35

The intracellular innate immune receptor NOD1 detects Gram-negative bacterial peptidoglycan (PG) to induce autophagy and inflammatory responses in host cells. To date, the intracellular compartment in which PG is detected by NOD1 and whether NOD1 directly interacts with PG are two questions that remain to be resolved. To address this, we used outer membrane vesicles (OMVs) from pathogenic bacteria as a physiological mechanism to deliver PG into the host cell cytosol. We report that OMVs induced autophagosome formation and inflammatory IL-8 responses in epithelial cells in a NOD1- and RIP2-dependent manner. PG contained within OMVs colocalized with both NOD1 and RIP2 in EEA1-positive early endosomes. Further, we provide evidence for direct interactions between NOD1 and PG. Collectively, these findings demonstrate that NOD1 detects PG within early endosomes, thereby promoting RIP2-dependent autophagy and inflammatory signaling in response to bacterial infection.

http://www.ncbi.nlm.nih.gov/pubmed/24746552