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miR-194b-3p partially inhibits Streptococcus equi subsp. zooepidemicus adherence to PK15 cells

Bin Tang1, Huihuang Liang1, Pengpeng Zhao1

  • 1Hubei Collaborative Innovation Center for Green Transformation of Bio-resources, College of LifeSciences, Hubei University, Wuhan, Hubei 430062, PR China.

Veterinary Microbiology
|November 7, 2017
PubMed

Insights

MicroRNAs regulate bacterial adhesion. This study found that miR-194b-3p inhibits Streptococcus equi subsp. Zooepidemicus (SeZ) adherence to porcine kidney cells by targeting CD44, revealing a key host-pathogen interaction mechanism.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Immunology

Background:

  • MicroRNAs (miRNAs) play crucial roles in host-pathogen interactions.
  • Understanding miRNA regulation in bacterial infections is vital for host defense mechanisms.

Purpose of the Study:

  • To investigate the role of miR-194b-3p in the adherence of Streptococcus equi subsp. Zooepidemicus (SeZ) to porcine kidney (PK15) cells.
  • To elucidate the molecular mechanism underlying this interaction.

Main Methods:

  • Transfection of miR-194b-3p agomir and antagomir into PK15 cells.
  • Determination of SeZ adherence rates to transfected PK15 cells.
  • Analysis of CD44 expression levels and its interaction with miR-194b-3p via the 3' UTR.

Main Results:

  • Transfection of miR-194b-3p agomir significantly decreased SeZ C55138 adherence to PK15 cells.
  • miR-194b-3p was confirmed to inhibit SeZ C55138 adherence.
  • miR-194b-3p directly targets CD44 3' UTR, influencing the adhesion process.

Conclusions:

  • miR-194b-3p acts as an inhibitor of SeZ C55138 adherence to PK15 cells.
  • The miR-194b-3p-CD44 interaction is a key factor in the host-pathogen crosstalk between SeZ and PK15 cells.
  • This finding contributes to understanding host immune responses to bacterial pathogens.
Keywords:
AdherenceMicroRNAPK15 cellsStreptococcus equi subsp. zooepidemicus

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