The intracellular status of Streptococcus pyogenes: role of extracellular matrix-binding proteins and their

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Invasion of Human Cells by a Bacterial Pathogen
07:15

Invasion of Human Cells by a Bacterial Pathogen

Published on: March 21, 2011

Bernd Kreikemeyer1, Michael Klenk, Andreas Podbielski

  • 1Department of Medical Microbiology and Hospital Hygiene, University Hospital Rostock, Schillingallee 70, D-18055 Rostock, Germany. bernd.kreikemeyer@med.uni-rostock.de

International Journal of Medical Microbiology : IJMM
|October 21, 2004
PubMed

Insights

Streptococcus pyogenes (GAS) uses microbial surface components (MSCRAMMs) to adhere to and enter host cells, establishing intracellular infections. Understanding these adherence mechanisms is key to developing new anti-infective strategies against GAS.

Area of Science:

  • Microbiology
  • Pathogenesis
  • Molecular Biology

Background:

  • Streptococcus pyogenes (group A streptococci, GAS) is a significant human pathogen.
  • Bacterial adherence and internalization into host cells are critical for GAS pathogenesis.
  • Extracellular matrix (ECM) proteins are key targets for GAS adherence.

Purpose of the Study:

  • To investigate the role of microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) in GAS adherence and internalization.
  • To understand the regulatory networks controlling MSCRAMM expression.
  • To identify potential targets for novel anti-infective strategies.

Main Methods:

  • Identification and characterization of GAS MSCRAMMs, such as protein F1/SfbI.
  • Analysis of the interaction between MSCRAMMs, ECM proteins (fibronectin, collagen), and host cell integrins.
  • Investigation of transcriptional regulators and two-component systems controlling MSCRAMM gene expression.
  • Study of GAS persistence in intracellular niches.

Main Results:

  • GAS utilizes MSCRAMMs to bind ECM proteins like fibronectin.
  • Bound fibronectin bridges GAS to host cell integrins, initiating bacterial internalization.
  • Internalized GAS can persist intracellularly, evading antibiotics and host defenses.
  • MSCRAMM expression is regulated by complex networks involving transcriptional regulators and pathogenicity islands, with strain-specific variations.

Conclusions:

  • GAS adherence and internalization mechanisms, mediated by MSCRAMMs, are crucial for establishing persistent intracellular infections.
  • Understanding the regulation of MSCRAMM expression offers a promising avenue for developing novel anti-infective therapies targeting GAS.
  • Targeting MSCRAMM function and regulatory pathways could combat treatment failure, asymptomatic carriage, and recurrent GAS infections.

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