Decreased expression alleviates beta2 toxin-induced inflammatory injury in IPEC-J2 cells.

BACKGROUND

S100 calcium-binding protein A9 (S100A9) is a commonly known pro-inflammatory factor involved in various inflammatory responses. ( ) type C is known to cause diarrhea in piglets. However, the role of in C-induced infectious diarrhea is unclear.

METHODS

Here, the gene was overexpressed and knocked down in the IPEC-J2 cells, which were treated with beta2 (CPB2) toxin. The role of in CPB2 toxin-induced injury in IPEC-J2 cells was assessed by measuring the levels of inflammatory cytokines, reactive oxygen species (ROS), lactate dehydrogenase (LDH), cell proliferation, and tight junction-related proteins.

RESULTS

The results showed elevated expression of in diarrhea-affected piglet tissues, and the elevation of expression after CPB2 toxin treatment of IPEC-J2 was time-dependent. In CPB2 toxin-induced IPEC-J2 cells, overexpression of had the following effects: the relative expression of inflammatory factors , , , and was increased; the ROS levels and LDH viability were significantly increased; cell viability and proliferation were inhibited; the G0/G1 phase cell ratio was significantly increased. Furthermore, overexpression of reduced the expression of tight junction proteins in CPB2-induced IPEC-J2 cells. The knockdown of had an inverse effect. In conclusion, our results confirmed that exacerbated inflammatory injury in CPB2 toxin-induced IPEC-J2 cells, inhibited cell viability and cell proliferation, and disrupted the tight junctions between cells. Thus, decreased expression alleviates CPB2 toxin-induced inflammatory injury in IPEC-J2 cells.