S100A12 is involved in the inflammatory response and is considered an important marker for many inflammatory diseases in humans. Our previous studies indicated that the
S100A12 gene was abundant in the immune tissues of pigs and was significantly upregulated during
infection with Haemophilus parasuis (HPS) or porcine circovirus type 2 (PCV2). In this study, the mechanism of transcriptional regulation of
S100A12 was investigated in pigs. Our results showed that
S100A12,
CCAAT/enhancer-binding protein beta (C/EBPβ) and
activator protein-1 (AP-1) genes were up-regulated in PK-15 (ATCC, CCL-33) cells when treated with LPS or
Poly I: C. Additionally, the promoter activity and expression level of the
S100A12 gene were significantly upregulated when C/EBPβ or
AP-1 were overexpressed. We utilized electromobility shift assays (EMSA) to confirm that C/EBPβ and
AP-1 could directly bind the
S100A12 gene promoter. We also found that the transcriptional activity and expression levels of C/EBPβ and
AP-1 could positively regulate each other. Furthermore, the promoter activity of the
S100A12 gene was higher when C/EBPβ and
AP-1 were cotransfected than when they were transfected individually. We concluded that the
S100A12 gene was cooperatively and positively regulated by C/EBPβ and
AP-1 in pigs. Our study offers new insight into the transcriptional regulation of the
S100A12 gene.