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Epithelial invasion by Salmonella Typhi using STIV-Met interaction.

Rimi Chowdhury1, Sayan Das1, Atri Ta1

  • 1Division of Clinical Medicine, National Institute of Cholera and Enteric Diseases, Kolkata, India.

Cellular Microbiology
|November 15, 2018
PubMed
Summary

Salmonella Typhi invasion uses outer membrane protein STIV to bind host Met receptor, activating signaling pathways for bacterial entry. This T3SS-1 independent mechanism offers a potential therapeutic target for typhoid fever.

Keywords:
MetSTIVSalmonella enterica serovar Typhireceptor-mediated endocytosis

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Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Typhoid fever, caused by Salmonella Typhi, is a severe febrile illness affecting millions globally.
  • Intestinal invasion by Salmonella Typhi is critical for infection, traditionally linked to the T3SS-1 secretion system.
  • Previous research identified outer membrane protein T2942/STIV as a potential independent invasin.

Purpose of the Study:

  • To elucidate the mechanism of T3SS-1-independent epithelial invasion by Salmonella Typhi.
  • To identify the host cell receptor and signaling pathway utilized by STIV for bacterial entry.

Main Methods:

  • Investigated the interaction between STIV and host intestinal epithelial cells.
  • Analyzed the role of receptor tyrosine kinase Met and downstream signaling molecules (Src, PI3K/Akt, Rac1).
  • Assessed the impact of Met tyrosine kinase inhibition on Salmonella Typhi invasion and systemic infection in vivo.

Main Results:

  • STIV interacts with the host Met receptor via its extracellular loop, triggering Met phosphorylation and activation.
  • This initiates a signaling cascade involving Src, PI3K/Akt, and Rac1, leading to actin polymerization and bacterial engulfment.
  • Inhibition of Met tyrosine kinase activity significantly reduced Salmonella Typhi intestinal invasion and systemic infection.

Conclusions:

  • This study reveals a novel T3SS-1-independent invasion pathway for Salmonella Typhi mediated by STIV and host Met receptor.
  • The identified host-pathogen interaction provides critical insights into typhoid pathogenesis.
  • Targeting this STIV-Met interaction presents a potential therapeutic strategy to combat Salmonella Typhi infections.