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An internal thioester in a pathogen surface protein mediates covalent host binding.

Miriam Walden1, John M Edwards2, Aleksandra M Dziewulska2

  • 1Department of Biological Chemistry, John Innes Centre, Norwich, United Kingdom.

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|June 3, 2015
PubMed
Summary

Pathogenic microbes use a novel covalent mechanism, mediated by the streptococcal surface protein SfbI, to attach to host tissues. This discovery reveals a new molecular principle in host-microbe interactions and potential therapeutic targets.

Keywords:
Clostridium perfringensStreptococcus pneumoniaeStreptococcus pyogenesbacterial surface proteinsbiophysicsfibrinogenhost-microbe interactionsinfectious diseasemicrobiologystructural biology

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Immunology

Background:

  • Bacterial adhesion to host tissues is crucial for colonization and disease.
  • Microbial surface proteins, known as adhesins, mediate these interactions.
  • Previously, all known adhesins were understood to bind host receptors non-covalently.

Purpose of the Study:

  • To investigate the molecular mechanism of bacterial adhesion.
  • To identify novel strategies for targeting bacterial infections.

Main Methods:

  • Characterization of the streptococcal surface protein SfbI.
  • Analysis of the interaction between SfbI and host protein fibrinogen.
  • In vitro assays to assess bacterial attachment and binding to human cells.

Main Results:

  • SfbI mediates a covalent interaction with host fibrinogen via an internal thioester bond, acting as a 'chemical harpoon'.
  • This covalent cross-linking facilitates bacterial attachment to fibrin and SfbI binding to human cells.
  • Thioester-containing domains are common in Gram-positive bacteria, including pathogens.

Conclusions:

  • Bacterial-encoded covalent binding represents a new molecular principle in host-microbe interactions.
  • This mechanism offers a potential new target for treating bacterial infections.
  • The findings may also inspire novel approaches for engineering beneficial host-microbe interactions.