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A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions
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Cadherin-mediated host-pathogen interactions.

Sagarika Dash1, Kheerthana Duraivelan1, Dibyendu Samanta1

  • 1School of Bioscience, Indian Institute of Technology Kharagpur, Kharagpur, India.

Cellular Microbiology
|February 5, 2021
PubMed
Summary

Microbial pathogens exploit cadherins, crucial cell adhesion molecules, to invade host cells. This review details how pathogens use virulence factors to disrupt cell junctions and trigger signaling for entry.

Keywords:
E-cadherinbacterial adhesinsbacterial virulence factorscell adhesion moleculesendocytosishost entry-receptors for pathogens

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Area of Science:

  • Cell Biology
  • Microbiology
  • Immunology

Background:

  • Cell adhesion molecules (CAMs) are vital for multicellular organism development, mediating cell-cell and cell-matrix interactions.
  • Cadherins, a major class of CAMs, work with nectins to form adherens junctions, essential for cell adhesion, communication, and signaling.
  • Recent research highlights cadherins' role in host-pathogen interactions, beyond their typical adhesive functions.

Purpose of the Study:

  • To review how microbial pathogens and their virulence factors exploit cadherins for host cell invasion.
  • To elucidate the molecular mechanisms underlying cadherin-mediated host-pathogen interactions.
  • To discuss the downstream signaling events, including endocytosis, triggered by microbial exploitation of cadherins.

Main Methods:

  • Literature review of studies on cadherins, microbial virulence factors, and host-pathogen interactions.
  • Analysis of macromolecular interactions between cadherins and microbial components (toxins, adhesins).
  • Examination of cell signaling pathways, including endocytosis, activated during microbial invasion.

Main Results:

  • Microbial pathogens utilize specific virulence factors to target and disrupt cadherin-based cell junctions.
  • Interactions between microbial toxins/adhesins and cadherins lead to junction disintegration, facilitating pathogen entry.
  • Pathogen invasion triggers host cell signaling cascades, including those involving the endocytosis machinery.

Conclusions:

  • Cadherins are critical targets for microbial invasion strategies, enabling pathogens to breach host defenses.
  • Understanding these molecular interactions provides insights into host-pathogen dynamics and potential therapeutic targets.
  • The review emphasizes the complex interplay between microbial factors, host cell adhesion machinery, and signaling pathways during infection.