Related Experiment Video

Updated: May 11, 2026

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
10:57

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells

Published on: January 12, 2020

Salmonella effector SteE reprograms the macrophage regulatory network to drive specific hyperactivation of STAT3

Ines Diaz-Del-Olmo1, Paul A O'Sullivan2, Thomas S Wilson3

  • 1Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK; Department of Infectious Disease, Centre for Bacterial Resistance Biology, Imperial College London, London SW7 2AZ, UK; Bacterial Pathogenesis and Immune Signalling Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.

Molecular Cell
|May 9, 2026
PubMed

Insights

Salmonella Typhimurium

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Salmonella Typhimurium utilizes macrophages for survival and dissemination.
  • The effector SteE is crucial for Salmonella pathogenesis by inducing an anti-inflammatory state in macrophages.

Purpose of the Study:

  • To investigate the mechanism by which SteE reprograms macrophages.
  • To determine the role of STAT3 phosphorylation and DNA binding in SteE-mediated immune evasion.

Main Methods:

  • Investigated SteE's interaction with host kinases.
  • Analyzed STAT3 phosphorylation and DNA binding activity.
  • Assessed gene expression and chromatin remodeling in macrophages.

Main Results:

  • SteE hijacks GSK3 to phosphorylate STAT3 via a non-canonical pathway.
  • SteE-induced STAT3 hyperactivation bypasses negative feedback loops.
  • This leads to enhanced expression of STAT3 target genes and immune evasion.

Conclusions:

  • SteE critically reprograms macrophage gene expression through STAT3 hyperactivation.
  • This mechanism enhances Salmonella's ability to evade the host immune response.
  • Targeting this pathway could offer novel therapeutic strategies against Salmonella infections.
Keywords:
STAT3SalmonellaSteEanti-inflammatoryeffectorgene regulatory networkhost-pathogen interactionsmacrophagevirulence factor

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