The Attenuated Brucella abortus Strain 19 Invades, Persists in, and Activates Human Dendritic Cells, and Induces the Secretion of IL-12p70 but Not IL-23.

Background: Bacterial vectors have been proposed as novel vaccine strategies to induce strong cellular immunity. Attenuated strains of Brucella abortus comprise promising vector candidates since they have the potential to induce strong CD4(+) and CD8(+) T-cell mediated immune responses in the absence of excessive inflammation as observed with other Gram-negative bacteria. However, some Brucella strains interfere with the maturation of dendritic cells (DCs), which is essential for antigen-specific T-cell priming.

Cytotoxic activity of murine resident peritoneal cells against Listeria monocytogenes-infected hepatocytes in vitro.

Sterile immunity to the Gram-positive facultative intracellular bacterium Listeria monocytogenes critically depends on cytotoxic CD8+ T lymphocytes. However, the cytotoxic cell population able to kill infected cells before specific T cells are generated is not well characterised. Based on histological observations and the use of monoclonal antibodies abrogating the CD11b/CD18-dependent cellular influx into infected organs as well as granulocyte-depleting antibodies, some authors favour PMNs as being most important in the preimmune lysis of L.

Tailoring host immune responses to Listeria by manipulation of virulence genes -- the interface between innate and acquired immunity.

Although attenuated strains of microbial pathogens have triggered vaccine development from its origin, the role of virulence factors in determining host immunity has remained largely unexplored. Using the murine listeriosis model, we investigated whether the induction and expansion of protective and inflammatory T cell responses may be modified by selective manipulation of virulence genes. We intentionally deleted specific genes of Listeria monocytogenes, including those encoding the positive regulatory factor (prfA), hemolysin (hly), the actin nucleator (actA), and phospholipase B (plcB).