Heat-stable enterotoxin induced apoptosis in small intestine epithelial cells via mitochondrial oxidative phosphorylation pathway
Year: 2025
Type: article
Abstract: Newborn piglet diarrhea caused by enterotoxigenic Escherichia coli (ETEC) causes serious economic losses in the swine industry worldwide. Heat-stable enterotoxins (STa) secreted by ETEC can damage the intestine, resulting in villus atrophy and shedding, which is the main cause of diarrhea in newborn piglets; however, the mechanism is not clear. This experiment was conducted in vivo (three-day-old suckling mice) and in vitro (IPEC-J2 cells) to explore the effect of STa on the intestinal epithelium by comparing the differences after infection with STa toxin-secreting E. coli O142 or STa-knockout E. coli O142ΔestA. The results showed that STa caused diarrhea, small intestinal edema, atrophy and rupture of small intestinal villi, and death in a dose-dependent manner in mice, and downregulated oxidative phosphorylation (OXPHOS) in IPEC-J2 cells. Activation of the mitochondria-mediated cell apoptosis pathway through excessive reactive oxygen species (ROS) production induces injury of the small intestinal villi, leading to diarrhea in piglets.
Source: Frontiers in Veterinary Science
Authors: Meijia Hou, Wei Yang, Nian Liu, Simeng Sun, Qizheng Feng, Bo Shi, Jiali Liu, Xiumei Dong
Institution: Northeast Agricultural University
Language: English
Subfield: Endocrinology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $3,801
Award: G7027315920
OpenAlex ID: W4410118633
