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PotD contributes to Streptococcus suis-induced blood-brain barrier disruption by regulating arcA transcription

Shiqi Lang1, Hang Yin1, Xiaoyu Jia1

  • 1Joint International Research Laboratory of Animal Health and Animal Food Safety, College of Veterinary Medicine, Southwest University, No.2 Tiansheng Road, Beibei District, Chongqing, 400715, China.

Veterinary Research
|December 2, 2025
PubMed

Insights

Streptococcus suis PotD protein contributes to bacterial pathogenicity and blood-brain barrier disruption by downregulating tight junction proteins. Deleting PotD enhances mouse survival and reduces bacterial load, revealing its role in S. suis virulence.

Area of Science:

  • Microbiology
  • Pathogenesis
  • Neuroscience

Background:

  • The role of ABC transporter substrate-binding protein PotD in Streptococcus suis pathogenicity, particularly in blood-brain barrier (BBB) disruption, remains unclear.
  • Streptococcus suis is a significant pathogen causing meningitis and sepsis.

Purpose of the Study:

  • To investigate the mechanism of PotD in mediating S. suis pathogenicity and BBB disruption.
  • To identify potential interactions of PotD with other virulence factors.

Main Methods:

  • Gene knockout (ΔpotD, ΔarcA) and complementation studies in S. suis.
  • Assessment of bacterial load, biofilm formation, and mouse survival rates.
  • In vitro assays using human cerebral microvascular endothelial cells (hCMEC/D3) to evaluate BBB integrity.
  • Analysis of tight junction proteins (ZO-1, Occludin) expression.
  • Mass spectrometry and pulldown assays to identify protein interactions.
  • Recombinant protein treatments (PotD, ADI) to assess direct effects on BBB.

Main Results:

  • Deletion of potD significantly reduced biofilm formation, bacterial load in tissues, and increased mouse survival.
  • PotD knockout reversed the downregulation of ZO-1 and Occludin, and attenuated BBB disruption.
  • Recombinant PotD protein directly disrupted the BBB by downregulating ZO-1 and Occludin.
  • PotD was found to interact with arginine deiminase (ADI) and mediate arcA transcription.
  • Deletion of arcA also attenuated BBB disruption, and recombinant ADI induced BBB disruption.

Conclusions:

  • PotD is a crucial virulence factor for S. suis, contributing to pathogenicity and BBB disruption.
  • PotD-induced BBB disruption involves the downregulation of tight junction proteins ZO-1 and Occludin.
  • PotD interacts with ADI, and both PotD and ADI play significant roles in S. suis-induced BBB damage.
  • These findings provide new insights into S. suis pathogenesis and potential therapeutic targets.
Keywords:
Streptococcus suisPotDarginine deiminase (ADI)blood–brain barrier (BBB)

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