THP-1 monocytes up-regulate intercellular adhesion molecule 1 in response to pneumolysin from Streptococcus

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Updated: Aug 15, 2026

Legionella pneumophila Outer Membrane Vesicles: Isolation and Analysis of Their Pro-inflammatory Potential on Macrophages
08:34

Legionella pneumophila Outer Membrane Vesicles: Isolation and Analysis of Their Pro-inflammatory Potential on Macrophages

Published on: February 22, 2017

Justin Thornton1, Larry S McDaniel

  • 1Department of Microbiology, University of Mississippi Medical Center, Jackson, 39216, USA,

Infection and Immunity
|September 24, 2005
PubMed

Insights

Pneumolysin (PLY) from Streptococcus pneumoniae increases the expression of Intercellular Adhesion Molecule 1 (ICAM-1) in immune cells. This suggests PLY plays a role in pneumococcal infection by modulating inflammatory responses.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Streptococcus pneumoniae utilizes pneumolysin (PLY) as a key virulence factor.
  • Intercellular Adhesion Molecule 1 (ICAM-1) is crucial for leukocyte recruitment during inflammation.

Purpose of the Study:

  • To investigate the impact of PLY on ICAM-1 expression in THP-1 monocytic cells.
  • To elucidate the role of PLY in modulating immune cell adhesion molecule expression during pneumococcal infections.

Main Methods:

  • Exposure of THP-1 cells to S. pneumoniae strains (PLY-expressing and PLY-deficient mutants).
  • Treatment of THP-1 cells with purified recombinant PLY and its variants.
  • Quantification of ICAM-1 mRNA and surface expression using molecular and cellular assays.

Main Results:

  • PLY-expressing S. pneumoniae significantly increased ICAM-1 mRNA levels compared to mutant strains.
  • Recombinant PLY induced a dose-dependent increase in ICAM-1 mRNA.
  • A non-lytic PLY mutant showed reduced ICAM-1 mRNA induction, indicating a role for PLY's activity.
  • Increased surface ICAM-1 expression was observed on THP-1 cells exposed to wild-type S. pneumoniae.

Conclusions:

  • Pneumolysin (PLY) directly induces the transcription and production of Intercellular Adhesion Molecule 1 (ICAM-1).
  • This PLY-mediated upregulation of ICAM-1 may contribute to the inflammatory processes observed in pneumococcal infections.
  • The findings highlight a specific mechanism by which S. pneumoniae manipulates host immune responses.

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