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Nontypeable Haemophilus influenzae P5 Binds Human C4b-Binding Protein, Promoting Serum Resistance

Oskar Thofte1, Serena Bettoni2, Yu-Ching Su1

  • 1Clinical Microbiology, Department of Translational Medicine, Faculty of Medicine, Lund University, Malmö, Sweden.

Journal of Immunology (Baltimore, Md. : 1950)
|August 26, 2021
PubMed

Insights

Nontypeable Haemophilus influenzae (NTHi) uses outer membrane protein 5 (P5) to bind complement-binding protein (C4BP), enhancing its survival. P5 expression is higher in severe respiratory infections, aiding NTHi immune evasion.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogen-host interactions

Background:

  • Nontypeable Haemophilus influenzae (NTHi) is a significant human pathogen causing respiratory infections.
  • NTHi evades the complement system, a crucial part of innate immunity, for survival.
  • Complement-binding protein (C4BP) binding is known to be important for NTHi complement evasion.

Purpose of the Study:

  • To identify novel NTHi surface proteins involved in complement evasion.
  • To investigate the role of outer membrane protein 5 (P5) in NTHi's interaction with C4BP.
  • To correlate P5 expression with C4BP binding and serum resistance in clinical isolates.

Main Methods:

  • Identification of NTHi outer membrane protein 5 (P5) as a C4BP ligand.
  • Construction and analysis of P5-deficient NTHi mutants.
  • Surface expression of recombinant P5 on Escherichia coli.
  • Correlation analysis of P5 expression and C4BP binding in clinical NTHi isolates.

Main Results:

  • NTHi outer membrane protein 5 (P5) was identified as a novel ligand for C4BP.
  • P5-deficient NTHi mutants showed reduced C4BP binding and decreased serum resistance.
  • Recombinant P5 expression on E. coli conferred C4BP binding and enhanced serum resistance.
  • P5 surface expression and C4BP binding levels were higher in isolates from lower respiratory tract infections and tonsils.

Conclusions:

  • Outer membrane protein 5 (P5) is a key factor for NTHi complement evasion.
  • P5 facilitates NTHi survival by promoting C4BP binding, thereby conferring resistance to complement-mediated killing.
  • P5 expression levels correlate with infection site, suggesting its importance in specific NTHi pathogenesis.

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