miR-194b-3p对马链球菌兽疫亚种粘附猪肾上皮细胞能力影响的研究

Study on the influence of miR-194b-3p on the adhesion ability of Streptococcus equi subsp. zooepidemicus to kidney epithelial cells of swine

microRNA分子在调节宿主细胞应对细菌感染的过程中起重要作用。为研究miR-194b-3p对马链球菌兽疫亚种(SeZ)粘附猪肾上皮细胞(PK15)能力的影响,本实验将miR-194b-3pagomir和antagomir分别转染PK15细胞,检测SeZ对PK15细胞粘附能力的变化。结果表明:在PK15细胞中转染miR-194b-3p agomir,SeZ C55138粘附率显著下降;转染miR-194b-3p antagomir,SeZ C55138粘附率显著上升,确定了miR-194b-3p能够显著抑制SeZ C55138对PK15细胞的粘附。同时对其机制进行研究,显示PK15细胞表面CD44是miR-194b-3p的一个调控靶基因,miR-194b-3p通过调节CD44的表达参与影响了上述粘附过程。本实验为深入理解SeZ与PK15细胞的互作机制提供了线索。

MicroRNAs are increasingly 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. The adherence rate of SeZ C55138 was significantly decreased when miR-194b-3p agomir was transfected into PK15, while the adherence rate was significantly increased when miR-1946-3p antagomir was transfected into PK15. These results confirmed that miR-194b-3p markedly inhibit the adherence of SEZC55138 to PK15 cells. In addition, miR-194b-3p indeed regulated the expression level of CD44 in PK15 cells, and this interaction was involved in adhesion process. This study contributed to understand the mechanism of the interaction between SeZ and PK15 cells.