Related Experiment Video

Updated: Jul 6, 2026

Analysis of Yersinia enterocolitica Effector Translocation into Host Cells Using Beta-lactamase Effector Fusions
12:23

Analysis of Yersinia enterocolitica Effector Translocation into Host Cells Using Beta-lactamase Effector Fusions

Published on: October 13, 2015

Crosstalk of signalling processes of innate immunity with Yersinia Yop effector functions

Klaus Ruckdeschel1, Anne Deuretzbacher, Rudolf Haase

  • 1Institute for Medical Microbiology, Virology and Hygiene, University Medical Center Eppendorf, Martinistr. 52, 20246 Hamburg, Germany. k.ruckdeschel@uke.uni-hamburg.de

Immunobiology
|April 15, 2008
PubMed

Insights

Yersinia bacteria inject toxins (Yops) into host cells, disrupting immune functions like phagocytosis and triggering macrophage death. This study details the molecular interplay governing host-pathogen interactions and immune response outcomes.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Infectious diseases arise from microbial pathogen-host cell interactions.
  • Gram-negative Yersinia bacteria deliver virulence proteins (Yops) into host cells.
  • Yops disrupt innate immunity, including phagocytosis, inflammatory signaling, and apoptosis in macrophages.

Purpose of the Study:

  • To explore the crosstalk between Yersinia pathogens and host cells.
  • To summarize current understanding of host-pathogen signaling.
  • To elucidate mechanisms determining host cell fate during Yersinia infection.

Main Methods:

  • Utilizing Yersinia enterocolitica as a model pathogen.
  • Analyzing Yop effector protein functions within host cells.
  • Investigating Toll-like receptor-dependent signaling pathways.

Main Results:

  • Yersiniae counteract host phagocytosis.
  • Pro-inflammatory signaling is suppressed by Yersinia infection.
  • Macrophage apoptosis is triggered by Yersinia, linked to signaling pathway deregulation.

Conclusions:

  • Yersinia infection profoundly impacts macrophage function and survival.
  • Deregulation of conserved signaling pathways by Yops is central to Yersinia pathogenesis.
  • Understanding these interactions is crucial for comprehending innate immune responses to bacterial pathogens.

More Related Videos

Quantifying Yersinia pseudotuberculosis Type III Secretion System Activity Following Iron Starvation and Anaerobic Growth08:36

Quantifying Yersinia pseudotuberculosis Type III Secretion System Activity Following Iron Starvation and Anaerobic Growth

Published on: May 31, 2024

Applying Fluorescence Resonance Energy Transfer (FRET) to Examine Effector Translocation Efficiency by Coxiella burnetii during siRNA Silencing10:29

Applying Fluorescence Resonance Energy Transfer (FRET) to Examine Effector Translocation Efficiency by Coxiella burnetii during siRNA Silencing

Published on: July 6, 2016

Related Concept Videos

Bacterial Signaling01:30

Bacterial Signaling

Bacterial signaling can occur within bacteria (intracellular) or between bacteria (intercellular). At times, a group of bacteria behaves like a community. To achieve this, they engage in quorum sensing, the perception of higher cell density that causes changes in gene expression. Quorum sensing involves both extracellular and intracellular signaling. The signaling cascade starts with a molecule called an autoinducer (AI). Individual bacteria produce AIs that move out of the bacterial cell...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Yeast Signaling01:28

Yeast Signaling

Yeasts are single-celled organisms, but unlike bacteria, they are eukaryotes (cells with a nucleus). Cell signaling in yeast is similar to signaling in other eukaryotic cells. A ligand, such as a protein or a small molecule released from a yeast cell, attaches to a receptor on the cell surface. The binding stimulates second-messenger kinases to activate or inactivate transcription factors that further regulate gene expression. Many of the yeast intracellular signaling cascades have similar...
Regulation of Bacterial Virulence01:28

Regulation of Bacterial Virulence

Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...