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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 : Journal of immunology (Baltimore, Md. : 1950)

Downregulation of the Na/K-ATPase pump by leptospiral glycolipoprotein activates the NLRP3 inflammasome

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Journal of immunology (Baltimore, Md. : 1950) - 08 Feb 2012

Lacroix-Lamandé S, d'Andon MF, Michel E, Ratet G, Philpott DJ, Girardin SE, Boneca IG, Vandewalle A, Werts C

Link to Pubmed [PMID] – 22323544

J. Immunol. 2012 Mar;188(6):2805-14

Leptospira interrogans is responsible for a zoonotic disease known to induce severe kidney dysfunction and inflammation. In this work, we demonstrate that L. interrogans induces NLRP3 inflammasome-dependent secretion of IL-1β through the alteration of potassium transport in bone marrow-derived macrophages. Lysosome destabilization also contributed to the IL-1β production upon stimulation with live, but not dead, bacteria. Using bone marrow-derived macrophages from various TLRs and nucleotide-binding oligomerization domain-deficient mice, we further determined that IL-1β production was dependent on TLR2 and TLR4, suggesting a participation of the leptospiral LPS to this process. Hypokaliemia in leptospirosis has been linked to the presence of glycolipoprotein, a cell wall component of L. interrogans that is known to inhibit the expression and functions of the Na/K-ATPase pump. We show in this study that glycolipoprotein activates the inflammasome and synergizes with leptospiral LPS to produce IL-1β, mimicking the effect of whole bacteria. These results were confirmed in vivo, as wild-type mice expressed more IL-1β in the kidney than TLR2/4-deficient mice 3 d postinfection with L. interrogans. Collectively, these findings provide the first characterization, to our knowledge, of bacteria-induced activation of the NLRP3 inflammasome through the downregulation of a specific host potassium transporter.

http://www.ncbi.nlm.nih.gov/pubmed/22323544