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

- miR-194b-3p markedly inhibit the adherence of SeZ C55138 to PK15 cells.
- miR-194b-3p did not influence the adherence of SeZ C55138 acapsular mutant to PK15 cells.
- miR-194b-3p indeed regulated the expression level of CD44 in PK15 cells.
- CD44-SeZ hyaluronic acid capsule interaction was involved in adhesion process between SeZ and PK15 cells.
- This study contributes to understanding the mechanism of the crosstalk between SeZ and PK15 cells.

MicroRNAs are increasingly reported implicated in the host cell response to bacterial pathogens. In order to investigate whether miR-194b-3p regulates the adherence of Streptococcus equi subsp. Zooepidemicus (SeZ) to porcine kidney cell line PK15, the miR-194b-3p agomir and antagomir were transfected into PK15 cells respectively and the adherence rate of SeZ to each was determined. Adherence rate of SeZ C55138 was significantly decreased when miR-194b-3p agomir was transfected in PK15, while that of miR-194b-3p antagomir evaluated. These results confirmed that miR-194b-3p markedly inhibit the adherence of SeZ C55138 to PK15 cells. In addition, miR-194b-3p indeed regulated the expression level of CD44 in PK15 cells by targeting CD44 3' UTR, and this interaction was involved in adhesion process. This study contributes to understanding the mechanism of the crosstalk between SeZ and PK15 cells.