S100A9 plays a key role in Clostridium perfringens beta2 toxin-induced inflammatory damage in porcine IPEC-J2 intestinal epithelial cells.
Jie LiKaihui XieJiaojiao YangJuanli ZhangQiaoli YangPengfei WangShuangbao GunXiaoyu HuangPublished in: BMC genomics (2023)
In conclusion, S100A9 was involved in CPB2-induced inflammatory response in IPEC-J2 cells by regulating the expression of downstream target genes, namely, TNF, CCL1, CCR7, CSF2, and CXCL9; promoting apoptosis; and aggravating oxidative cell damage. This study laid the foundation for further study on the regulatory mechanism underlying piglet diarrhea.
Keyphrases
- oxidative stress
- inflammatory response
- cell cycle arrest
- diabetic rats
- induced apoptosis
- high glucose
- poor prognosis
- escherichia coli
- rheumatoid arthritis
- endoplasmic reticulum stress
- stem cells
- cell therapy
- single cell
- dendritic cells
- gene expression
- genome wide
- regulatory t cells
- transcription factor
- mesenchymal stem cells
- endothelial cells
- immune response
- long non coding rna
- toll like receptor
- bone marrow
- stress induced