Omp25‐dependent engagement of SLAMF1 by Brucella abortus in dendritic cells limits acute inflammation and favours bacterial persistence in vivo

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 b...

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Bibliographic Details
Published in:Cellular microbiology 2020-04, Vol.22 (4), p.e13164-n/a
Main Authors: Degos, Clara, Hysenaj, Lisiena, Gonzalez‐Espinoza, Gabriela, Arce‐Gorvel, Vilma, Gagnaire, Aurélie, Papadopoulos, Alexia, Pasquevich, Karina Alejandra, Méresse, Stéphane, Cassataro, Juliana, Mémet, Sylvie, Gorvel, Jean‐Pierre
Format: Article
Language:English
Subjects:
acute and chronic infection
Animals
Bacteria
Bacterial Outer Membrane Proteins - genetics
Bacterial Outer Membrane Proteins - metabolism
Brucella
Brucella abortus
Brucella abortus - genetics
Brucella abortus - immunology
Brucella abortus - pathogenicity
CD150
Cell activation
Chronic infection
Cytokines
Dendritic cells
Dendritic Cells - immunology
Dendritic Cells - microbiology
Female
Host-Pathogen Interactions - immunology
Immune response
Immune system
Immunity, Innate
Infections
Inflammation
Innate immunity
Intracellular
Life Sciences
Membrane proteins
Mice
Mice, Inbred C57BL
Mice, Knockout
Mutation
NF‐κB
Omp25
Outer membrane proteins
Protein Binding
Proteins
Replication
Signaling Lymphocytic Activation Molecule Family Member 1 - genetics
Signaling Lymphocytic Activation Molecule Family Member 1 - metabolism
SLAMF1
Translocation
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Summary: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.
ISSN:1462-5814
1462-5822
DOI:10.1111/cmi.13164