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International audience; Legionella pneumophila is a pathogenic bacterium involved in regular outbreaks characterized by a relatively high fatality rate and an important societal impact. Frequent monitoring of the presence of this bacterium in environmental water samples is necessary to prevent these epidemic events, but the traditional culture-based detection and identification method requires up to 10 days. Reported herein is a method allowing identification of Legionella pneumophila by metabolic lipopolysaccharide labeling which targets, for the first time, a precursor to monosaccharides that are specifically present within the O-antigen of the bacterium. This new approach allows easy detection of living Legionella pneumophila, while other Legionella species are not labeled.

Brucellaspecies are responsible for the global zoonotic disease brucellosis. These intracellular pathogens express a set of factors – including lipopolysaccharides, virulence regulator proteins and phosphatidylcholine – to ensure their full virulence. Some virulence factors are essential for invasion of the host cell, whereas others are crucial to avoid elimination by the host. They allowBrucellaspp. to survive and proliferate within its replicative vacuole and enable the bacteria to escape detection by the host immune system. Several strategies have been used to develop animal vaccines against brucellosis, but no adequate vaccine yet exists to cure the disease in humans. This is probably due to the complicated pathophysiology of humanBrucellaspp. infection, which is different than in animal models. Here we reviewBrucellaspp. virulence factors and how they control bacterial trafficking within the host cell.

Brucella is an intracellular pathogen able to persist for long periods of time within the host and establish a chronic disease. We show that soon after Brucella inoculation in intestinal loops, dendritic cells from ileal Peyer's patches become infected and constitute a cell target for this pathogen. In vitro, we found that Brucella replicates within dendritic cells and hinders their functional activation. In addition, we identified a new Brucella protein Btp1, which down-modulates maturation of infected dendritic cells by interfering with the TLR2 signaling pathway. These results show that intracellular Brucella is able to control dendritic cell function, which may have important consequences in the development of chronic brucellosis., Author Summary A key determinant for intracellular pathogenic bacteria to induce infectious diseases is their ability to avoid recognition by the host immune system. Although most microorganisms internalized by host cells are efficiently cleared, Brucella behave as a Trojan horse causing a zoonosis called brucellosis that affects both humans and animals. Here we show that pathogenic Brucella are able to target host cell defense mechanisms by controlling the function of the sentinels of the immune system, the dendritic cells. In particular, the Brucella TIR-containing protein (Btp1) targets the Toll-like receptor 2 activation pathway, which is a major host response system involved in bacterial recognition. Btp1 is involved in the inhibition of dendritic cell maturation. The direct consequence is a control of inflammatory cytokine secretion and antigen presentation to T lymphocytes. These bacterial proteins are not specific for Brucella and have been identified in other pathogens and may be part of a general virulence mechanism used by several intracellular pathogens to induce disease.