Decreased S100A9 expression alleviates Clostridium perfringens beta2 toxin-induced inflammatory injury in IPEC-J2 cells

Bibliographic Details
Title: Decreased S100A9 expression alleviates Clostridium perfringens beta2 toxin-induced inflammatory injury in IPEC-J2 cells
Authors: Jie Li, Xiaoyu Huang, Kaihui Xie, Juanli Zhang, Jiaojiao Yang, Zunqiang Yan, Shuangbao Gun
Source: PeerJ, Vol 11, p e14722 (2023)
Publisher Information: PeerJ Inc., 2023.
Publication Year: 2023
Collection: LCC:Medicine
LCC:Biology (General)
Subject Terms: S100A9 gene, Piglet diarrhea, Clostridium perfringens type C, Clostridium perfringens beta2 toxin, Inflammatory injury, Medicine, Biology (General), QH301-705.5
More Details: Background S100 calcium-binding protein A9 (S100A9) is a commonly known pro-inflammatory factor involved in various inflammatory responses. Clostridium perfringens (C. perfringens ) type C is known to cause diarrhea in piglets. However, the role of S100A9 in C. perfringens type C-induced infectious diarrhea is unclear. Methods Here, the S100A9 gene was overexpressed and knocked down in the IPEC-J2 cells, which were treated with C. perfringens beta2 (CPB2) toxin. The role of S100A9 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 S100A9 in diarrhea-affected piglet tissues, and the elevation of S100A9 expression after CPB2 toxin treatment of IPEC-J2 was time-dependent. In CPB2 toxin-induced IPEC-J2 cells, overexpression of S100A9 had the following effects: the relative expression of inflammatory factors IL-6, IL8, TNF-α, and IL-1β 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 S100A9 reduced the expression of tight junction proteins in CPB2-induced IPEC-J2 cells. The knockdown of S100A9 had an inverse effect. In conclusion, our results confirmed that S100A9 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 S100A9 expression alleviates CPB2 toxin-induced inflammatory injury in IPEC-J2 cells.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2167-8359
Relation: https://peerj.com/articles/14722.pdf; https://peerj.com/articles/14722/; https://doaj.org/toc/2167-8359
DOI: 10.7717/peerj.14722
Access URL: https://doaj.org/article/3532b11588b640d6b8dd430772d23d99
Accession Number: edsdoj.3532b11588b640d6b8dd430772d23d99
Database: Directory of Open Access Journals
More Details
ISSN:21678359
DOI:10.7717/peerj.14722
Published in:PeerJ
Language:English