Abstract
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.
Highlights
The immune response to bacterial infection relies on the combined action of both the innate and adaptive immune systems
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
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
Summary
The immune response to bacterial infection relies on the combined action of both the innate and adaptive immune systems. Microbial stimuli induce significant morphological and biochemical changes, such as IL-12 secretion and increased surface expression of many costimulatory and MHC class II molecules This activation of DCs, known as maturation, is required for efficient T-cellpriming and pathogen elimination. Several studies have shown that while Salmonella typhimurium induces normal maturation of DCs and secretion of pro-inflammatory cytokines [3,4] it is able to block MHC class II antigen presentation in bone marrow-derived DCs [5,6] Another bacterial pathogen, Francisella tularensis, which induces phenotypic maturation of DCs, has been shown to inhibit secretion of pro-inflamatory cytokines such as TNF-a while eliciting production of immunosuppressive cytokines that facilitate pulmonary infection [7]. F. tularensis has been shown to replicate efficiently within DCs [7] in contrast to many other bacterial pathogens (including mycobacteria, Bordetella, Salmonella and Legionella pneumophila) for which DCs seem to restrict their intracellular growth
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