Brucella Egresses from Host Cells Exploiting Multivesicular Bodies.

Host cell egress is a critical step in the life cycle of intracellular pathogens, especially in microbes capable of establishing chronic infections. The Gram-negative bacterium Brucella belongs to such a group of pathogens. Even though much has been done to understand how Brucella avoids killing and multiplies in its intracellular niche, the mechanism that this bacterium deploys to egress from the cell to complete its cycle has been poorly studied.

VirJ Is a Brucella Virulence Factor Involved in the Secretion of Type IV Secreted Substrates.

The VirB secretion apparatus in Brucella belongs to the type IV secretion systems present in many pathogenic bacteria and is absolutely necessary for the efficient evasion of the Brucella-containing vacuole from the phagocytic route in professional phagocytes. This system is responsible for the secretion of a plethora of effector proteins that alter the biology of the host cell and promote the intracellular replication process. Although many VirB substrates have been identified in Brucella, we still know very little about the secretion mechanism that mediates their translocation across the two membranes and the periplasmic space.

Delta-pgm, a new live-attenuated vaccine against Brucella suis.

Brucellosis is one of the most widespread zoonosis in the world affecting many domestic and wild animals including bovines, goats, pigs and dogs. Each species of the Brucella genus has a particular tropism toward different mammals being the most relevant for human health Brucella abortus, Brucella melitensis and Brucella suis that infect bovines, goats/camelids and swine respectively. Although for B.

BigA is a novel adhesin of Brucella that mediates adhesion to epithelial cells.

Adhesion to cells is the initial step in the infectious cycle of basically all pathogenic bacteria, and to do so, microorganisms have evolved surface molecules that target different cellular receptors. Brucella is an intracellular pathogen that infects a wide range of mammals whose virulence is completely dependent on the capacity to replicate in phagocytes. Although much has been done to elucidate how Brucella multiplies in macrophages, we still do not understand how bacteria invade epithelial cells to perform a replicative cycle or what adhesion molecules are involved in the process.

A B lymphocyte mitogen is a Brucella abortus virulence factor required for persistent infection.

Microbial pathogens with the ability to establish chronic infections have evolved strategies to actively modulate the host immune response. Brucellosis is a disease caused by a Gram-negative intracellular pathogen that if not treated during the initial phase of the infection becomes chronic as the bacteria persist for the lifespan of the host. How this pathogen and others achieve this action is a largely unanswered question.