Mechanisms used by virulent Salmonella to impair dendritic cell function and evade adaptive immunity

Abstract

Summary Innate and adaptive immunity are inter‐related by dendritic cells (DCs), which directly recognize bacteria through the binding of pathogen‐associated molecular patterns (PAMPs) to specialized receptors on their surface. After capturing and degrading bacteria, DCs present their antigens as small peptides bound to MHC molecules and prime naive bacteria‐specific T cells. In response to PAMP recognition DCs undergo maturation, which is a phenotypic change that increases their immunogenicity and promotes the activation of naive T cells. As a result, a specific immune response that targets bacteria‐derived antigens is initiated. Therefore, the characterization of DC–bacteria interactions is important to understand the mechanisms used by virulent bacteria to avoid adaptive immunity. Furthermore, any impairment of DC function might contribute to bacterial survival and dissemination inside the host. An example of a bacterial pathogen capable of interfering with DC function is Salmonella enterica serovar Typhimurium (S. Typhimurium). Virulent strains of this bacterium are able to differentially modulate the entrance to DCs, avoid lysosomal degradation and prevent antigen presentation on MHC molecules. These features of virulent S. Typhimurium are controlled by virulence proteins, which are encoded by pathogenicity islands. Modulation of DC functions by these gene products is supported by several studies showing that pathogenesis might depend on this attribute of virulent S. Typhimurium. Here we discuss some of the recent data reported by the literature showing that several virulence proteins from Salmonella are required to modulate DC function and the activation of host adaptive immunity.

Increased S-Nitrosylation and Proteasomal Degradation of Caspase-3 during Infection Contribute to the Persistence of Adherent Invasive Escherichia coli (AIEC) in Immune Cells

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Salmonella Pathogenicity and Host Adaptation in Chicken-Associated Serovars

“…Salmonella cells have been shown to be able to multiply within macrophages (64) but do not appear to replicate within dendritic cells, even though they remain viable (60). The exact mechanisms for the differences in Salmonella responses within different immune cell types are not entirely clear, as several pathogen and host factors may play roles (65). Dendritic cells are widely distributed in the lymphoid and nonlymphoid tissues and can rapidly facilitate the spread of Salmonella cells to various organs of the host body (66).…”

Probiotic bacteria prevent Salmonella – induced suppression of lymphoproliferation in mice by an immunomodulatory mechanism

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