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Omp25‐dependent engagement of SLAMF1 by Brucella abortus in dendritic cells limits acute inflammation and favours bacterial persistence in vivo
Authors:Clara Degos,Lisiena Hysenaj,Gabriela Gonzalez‐Espinoza,Vilma Arce‐Gorvel,Aur  lie Gagnaire,Alexia Papadopoulos,Karina Alejandra Pasquevich,St  phane M  resse,Juliana Cassataro,Sylvie M  met,Jean‐Pierre Gorvel
Affiliation:Clara Degos,Lisiena Hysenaj,Gabriela Gonzalez‐Espinoza,Vilma Arce‐Gorvel,Aurélie Gagnaire,Alexia Papadopoulos,Karina Alejandra Pasquevich,Stéphane Méresse,Juliana Cassataro,Sylvie Mémet,Jean‐Pierre Gorvel
Abstract:The strategies by which intracellular pathogenic bacteria manipulate innate immunity to establish chronicity are poorly understood. Here, we show that Brucella abortus outer membrane protein Omp25 specifically binds the immune cell receptor SLAMF1 in vitro. The Omp25‐dependent engagement of SLAMF1 by B. abortus limits NF‐κB translocation in dendritic cells (DCs) with no impact on Brucella intracellular trafficking and replication. This in turn decreases pro‐inflammatory cytokine secretion and impairs DC activation. The Omp25‐SLAMF1 axis also dampens the immune response without affecting bacterial replication in vivo during the acute phase of Brucella infection in a mouse model. In contrast, at the chronic stage of infection, the Omp25/SLAMF1 engagement is essential for Brucella persistence. Interaction of a specific bacterial protein with an immune cell receptor expressed on the DC surface at the acute stage of infection is thus a powerful mechanism to support microbe settling in its replicative niche and progression to chronicity.
Keywords:acute and chronic infection     Brucella  CD150  dendritic cells  inflammation  NF‐κ  B  Omp25  SLAMF1
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