The strategies by which intracellular pathogenic bacteria manipulate innate immunity to establish chronicity are poorly understood. Here we show that B. 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 (DC) 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. This article is protected by copyright. All rights reserved.

中文翻译：

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树突状细胞中布鲁氏菌流产SLAMF1的Omp25依赖性参与限制了急性炎症并有利于体内细菌的持久性。

细胞内病原细菌操纵先天免疫以建立慢性的策略知之甚少。在这里，我们显示流产双歧杆菌外膜蛋白Omp25在体外特异性结合免疫细胞受体SLAMF1。流产芽孢杆菌对SLAMF1的Omp25依赖性参与限制了树突状细胞（DC）中的NF-κB转运，而对布鲁氏菌胞内运输和复制没有影响。反过来，这会减少促炎性细胞因子的分泌，并损害DC激活。Omp25-SLAMF1轴还可以减轻免疫反应，而不会在小鼠模型中布鲁氏菌感染的急性期影响体内细菌的复制。相反，在感染的慢性阶段，Omp25 / SLAMF1的参与对于布鲁氏菌的持久性至关重要。因此，在感染的急性阶段，特定细菌蛋白与DC表面表达的免疫细胞受体的相互作用是一种强大的机制，可支持微生物在其复制生态位中沉降并发展为慢性。本文受版权保护。版权所有。