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 |