Abstract

The adhesion of bacterial pathogens to host cells is an event that determines infection, and ultimately invasion and intracellular multiplication. Several evidences have recently shown that this rule is also truth for the intracellular pathogen Brucella. Brucella suis displays the unipolar BmaC and BtaE adhesins, which belong to the monomeric and trimeric autotransporter (TA) families, respectively. It was previously shown that these adhesins are involved in bacterial adhesion to host cells and components of the extracellular matrix (ECM). In this work we describe the role of a new member of the TA family of B. suis (named BtaF) in the adhesive properties of the bacterial surface. BtaF conferred the bacteria that carried it a promiscuous adhesiveness to various ECM components and the ability to attach to an abiotic surface. Furthermore, BtaF was found to participate in bacterial adhesion to epithelial cells and was required for full virulence in mice. Similar to BmaC and BtaE, the BtaF adhesin was expressed in a small subpopulation of bacteria, and in all cases, it was detected at the new pole generated after cell division. Interestingly, BtaF was also implicated in the resistance of B. suis to porcine serum. Our findings emphasize the impact of TAs in the Brucella lifecycle.

Highlights

  • Species from the Brucella genus are Gram negative bacteria, facultative intracellular pathogens responsible for brucellosis, a zoonotic disease that affects several terrestrial and marine mammals, including livestock [1]

  • We have previously shown that the passenger domain of BtaE comprises several repetitions of two motifs associated with adhesion (Fig. 1) [20]

  • Since infection of macrophages is crucial in the spread and persistence of Brucella spp. in the infected mammal [5,6], we evaluated whether BtaE and/or BtaF contribute to adhesion or invasion to professional phagocytes using as model the murine macrophage cell line J774

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Summary

Introduction

Species from the Brucella genus are Gram negative bacteria, facultative intracellular pathogens responsible for brucellosis, a zoonotic disease that affects several terrestrial and marine mammals, including livestock [1]. It is accepted that a low activation of the innate immunity for a long incubation period opens an immunological window that gives the opportunity to brucellae to spread throughout the reticuloendothelial system and establish the intracellular replication niche. After this long incubation period, a strong adaptive immunity is induced and the clinical symptoms are evident [5]. The virulence of Brucella spp. depends on their ability to replicate and survive within macrophages and other host cells, including epithelial cells, in a compartment derived from the endoplasmic reticulum [10,11,12,13]

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