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Streptococcus pneumoniae Interacts with pIgR expressed by the brain microvascular endothelium but does not

Federico Iovino1, Grietje Molema2, Jetta J E Bijlsma1

  • 1Department of Medical Microbiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.

Plos One
|May 21, 2014
PubMed

Insights

Streptococcus pneumoniae does not directly bind to platelet activating factor receptor (PAFR) on brain endothelial cells. Instead, the study reveals Polymeric immunoglobulin receptor (pIgR) as a potential novel adhesion receptor for pneumococci on the blood-brain barrier.

Area of Science:

  • Neuroscience
  • Microbiology
  • Immunology

Background:

  • Streptococcus pneumoniae adhesion to the blood-brain barrier (BBB) endothelium is a critical step in meningitis development.
  • Platelet activating factor receptor (PAFR) has been suggested to mediate this adhesion, but direct evidence is lacking, and alternative receptors are suspected.

Purpose of the Study:

  • To investigate the roles of PAFR and Polymeric immunoglobulin receptor (pIgR) in pneumococcal adhesion to brain endothelial cells in vivo.
  • To determine if PAFR or pIgR serve as direct binding sites for Streptococcus pneumoniae on the BBB endothelium.

Main Methods:

  • In vivo studies using a mouse model infected with Streptococcus pneumoniae, followed by immunofluorescent analysis of brain tissue.
  • In vitro experiments involving antibody blocking and incubation of bacteria with endothelial cell lysates to assess receptor interactions.

Main Results:

  • Streptococcus pneumoniae did not co-localize with PAFR in vivo or in vitro.
  • A majority of S. pneumoniae co-localized with endothelial pIgR.
  • Blocking pIgR significantly reduced pneumococcal adhesion to endothelial cells.
  • Physical interaction between pneumococci and pIgR was observed in endothelial cell lysates.

Conclusions:

  • PAFR plays an indirect role in pneumococcal adhesion to endothelial cells.
  • Endothelial pIgR represents a potential novel receptor for Streptococcus pneumoniae adhesion at the BBB.
  • These findings challenge the established role of PAFR and highlight pIgR as a new target for therapeutic intervention.

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