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Assays for Studying the Role of Vitronectin in Bacterial Adhesion and Serum Resistance
10:55

Assays for Studying the Role of Vitronectin in Bacterial Adhesion and Serum Resistance

Published on: October 16, 2018

Meningococcal surface fibril (Msf) binds to activated vitronectin and inhibits the terminal complement pathway to

Natalie J Griffiths1, Darryl J Hill, Elena Borodina

  • 1Schools of Cellular & Molecular Medicine, University of Bristol, Bristol BS8 1TD, UK.

Molecular Microbiology
|November 5, 2011
PubMed

Insights

Neisseria meningitidis uses a novel protein, Msf, to bind activated vitronectin, enhancing its survival against the human complement system. This binding mechanism provides serum resistance, crucial for meningococcal pathogenesis.

Area of Science:

  • Microbiology
  • Immunology
  • Bacterial Pathogenesis

Background:

  • Neisseria meningitidis (Nm) employs complement evasion for survival during infection.
  • The Nm adhesin Opc binds serum vitronectin to inhibit complement-mediated killing.
  • Vitronectin is a key serum protein involved in immune responses and coagulation.

Purpose of the Study:

  • To identify and characterize novel meningococcal adhesins involved in vitronectin binding.
  • To elucidate the mechanism by which meningococcal adhesins mediate complement resistance.
  • To assess the role of vitronectin binding in meningococcal pathogenesis and survival.

Main Methods:

  • Bacterial surface protein characterization and binding assays.
  • Analysis of complement-mediated killing and serum resistance.
  • In vitro and in vivo competition assays using bacterial mutants.
  • Peptide-based inhibition of protein-vitronectin interactions.

Main Results:

  • A novel adhesin, meningococcal surface fibril (Msf), mediates binding to activated vitronectin (aVn).
  • Both Msf and Opc bind aVn, conferring serum resistance, with enhanced resistance in co-expressing strains.
  • Blocking Msf-aVn interactions reversed aVn-mediated inhibition of complement component C5b-9 formation and serum killing.
  • Mutants lacking Msf or Opc were depleted in mixed population survival studies, indicating their importance for fitness.

Conclusions:

  • Meningococcal surface fibril (Msf) is a novel adhesin that binds activated vitronectin, contributing to serum resistance.
  • Vitronectin binding represents a significant survival strategy for Neisseria meningitidis, with redundant mechanisms (Opc and Msf) evolved for pathogenesis.
  • Targeting Msf-vitronectin interactions could be a potential therapeutic strategy against meningococcal infections.

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