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Expression and functional properties of the Streptococcus intermedius surface protein antigen I/II

F C Petersen1, S Pasco, J Ogier

  • 1Department of Oral Biology, Dental Faculty, University of Oslo, Blindern, N0372 Oslo, Norway. cpaiva@odont.uio.no

Infection and Immunity
|June 13, 2001
PubMed

Insights

Streptococcus intermedius antigen I/II is crucial for bacterial adhesion to human fibronectin and laminin. This surface protein also plays a key role in inducing interleukin-8 (IL-8) release from monocytes.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis

Background:

  • Streptococcus intermedius is a pathogen frequently linked to deep-seated purulent infections.
  • Antigen I/II is a surface protein found in various streptococci, often implicated in virulence.

Purpose of the Study:

  • To investigate the expression and functional roles of antigen I/II in Streptococcus intermedius.
  • To determine the involvement of antigen I/II in bacterial adhesion and host immune response.

Main Methods:

  • Gene expression analysis using Northern blotting.
  • Construction of an isogenic mutant by insertional inactivation of the antigen I/II gene.
  • Assessment of bacterial adhesion to extracellular matrix proteins and induction of cytokine release from monocytic cells.

Main Results:

  • Streptococcus intermedius antigen I/II is a cell surface-associated protein of approximately 160 kDa, with maximal gene expression during the early exponential growth phase.
  • The antigen I/II mutant exhibited reduced hydrophobicity and significantly decreased binding to human fibronectin and laminin.
  • The isogenic mutant showed a markedly reduced capacity to induce interleukin-8 (IL-8) release from THP-1 monocytic cells compared to the wild type.

Conclusions:

  • Streptococcus intermedius antigen I/II is a significant virulence factor involved in bacterial adhesion to host extracellular matrix components.
  • Antigen I/II contributes to the induction of the pro-inflammatory cytokine IL-8, suggesting a role in host immune modulation during infection.

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