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Glycosaminoglycan binding facilitates entry of a bacterial pathogen into central nervous systems

Yung-Chi Chang1, Zhipeng Wang, Lindsay A Flax

  • 1Glycobiology Research and Training Center, University of California, San Diego, La Jolla, California, United States of America.

Plos Pathogens
|July 7, 2011
PubMed

Insights

Group B Streptococcus uses glycosaminoglycan (GAG) interactions to invade the central nervous system. Targeting these bacterial-GAG interactions may offer new therapies for meningitis and other CNS infections.

Area of Science:

  • Microbiology
  • Neuroscience
  • Infectious Diseases

Background:

  • Certain microbes breach the blood-brain barrier (BBB) by invading brain microvascular endothelial cells (BMECs).
  • Group B Streptococcus (GBS) is a leading cause of meningitis and central nervous system (CNS) infection.

Purpose of the Study:

  • To investigate the role of glycosaminoglycan (GAG) interactions in GBS entry into the CNS.
  • To explore GAG-binding domains of GBS surface proteins as potential therapeutic targets.

Main Methods:

  • Utilized insect (Drosophila) and mammalian infection models.
  • Employed site-directed mutagenesis of the GAG-binding domain of GBS alpha C protein.
  • Assessed GBS adherence and invasion of human BMECs in vitro.
  • Genetically impaired GAG expression in model organisms.

Main Results:

  • Mutagenesis of the GAG-binding domain impeded GBS penetration of the Drosophila BBB and reduced adherence/invasion of human BMECs.
  • Impaired GAG expression in flies and mice decreased GBS dissemination into the brain.
  • Bacterial-GAG interactions were identified as crucial for CNS infection pathogenesis.

Conclusions:

  • Bacterial-GAG interactions play a significant role in the pathogenesis of CNS infections like meningitis.
  • Drosophila serves as a valuable model for screening therapeutic molecules targeting pathogen-GAG interactions.
  • Interruption of GAG-binding domains presents a potential strategy for preventing CNS entry of pathogens.

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