Dataset Information

YshB Promotes Intracellular Replication and Is Required for Salmonella Virulence.

ABSTRACT: Salmonella virulence requires the initial invasion of host cells, followed by modulation of the intracellular environment for survival and replication. In an effort to characterize the role of small RNAs in Salmonella pathogenesis, we inadvertently identified a 5-kDa protein named YshB that is involved in the intracellular survival of Salmonella We show here that yshB expression is upregulated upon entry into macrophages. When yshB expression is upregulated before bacterial entry, invasion efficiency is inhibited. Lack of YshB resulted in reduced bacterial survival within the macrophages and led to reduced virulence in a mouse model of infection.IMPORTANCE Salmonella gastroenteritis is one of the most common causes of foodborne disease, possibly affecting millions of people globally each year. Here we characterize the role of a novel small protein, YshB, in mediating Salmonella intracellular survival. This elucidation adds to the body of knowledge regarding how this bacterium achieves intracellular survival.

SUBMITTER: Bomjan R

PROVIDER: S-EPMC6689311 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

YshB Promotes Intracellular Replication and Is Required for Salmonella Virulence.

Bomjan Rajdeep R Zhang Mei M Zhou Daoguo D

Journal of bacteriology 20190808 17

Salmonella virulence requires the initial invasion of host cells, followed by modulation of the intracellular environment for survival and replication. In an effort to characterize the role of small RNAs in Salmonella pathogenesis, we inadvertently identified a 5-kDa protein named YshB that is involved in the intracellular survival of Salmonella We show here that yshB expression is upregulated upon entry into macrophages. When yshB expression is upregulated bef ...[more]

PMID: 31182500

Similar Datasets

Project description:Salmonella is one of the most important enteric pathogens worldwide, which is able to cause lethal systemic infection via survival and replication in host macrophages. Lactate, a byproduct of anaerobic or aerobic glycolysis, can induce macrophage M2 polarization, but the relationship between lactate-mediated macrophage M2 polarization and bacterial infection is poorly understood. Here, we evaluated the role of lactate and lactate-mediated macrophage M2 polarization in the pathogenicity of Salmonella. We found that lactate levels were significantly increased in Salmonella-infected macrophages, and the increased lactate was derived from the host. Macrophage and mouse infection assays showed that the addition of lactate enhanced Salmonella replication within macrophages and the colonization of mouse systemic loci, while pharmacological or genetic inhibition of host lactate production impaired Salmonella intracellular replication and its virulence in mice. Further analysis revealed that lactate promotes M2 polarization of Salmonella-infected macrophages, and the induction of macrophage M2 polarization by lactate is responsible for lactate-mediated Salmonella growth promotion. Moreover, we showed that macrophage-derived lactate induces the Salmonella pathogenicity island (SPI)-2 type III secretion system, leading to increased translocation of the SPI-2 effector SteE, which is responsible for driving M2 polarization. Overall, these findings suggest that lactate promotes Salmonella intracellular replication and systemic infection via driving macrophage M2 polarization and highlight the complex interactions between Salmonella and macrophages. IMPORTANCE The important enteropathogen Salmonella can cause lethal systemic infection via survival and replication in host macrophages. Lactate represents an abundant intracellular metabolite during bacterial infection, which can also induce macrophage M2 polarization. In this study, we found that macrophage-derived lactate promotes the intracellular replication and systemic infection of Salmonella. During Salmonella infection, lactate via the Salmonella type III secretion system effector SteE promotes macrophage M2 polarization, and the induction of macrophage M2 polarization by lactate is responsible for lactate-mediated Salmonella growth promotion. This study highlights the complex interactions between Salmonella and macrophages and provides an additional perspective on host-pathogen crosstalk at the metabolic interface.

Dataset Information

YshB Promotes Intracellular Replication and Is Required for Salmonella Virulence.

Publications

YshB Promotes Intracellular Replication and Is Required for <i>Salmonella</i> Virulence.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets