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Protective effect of Bombyx morigloverin on intestinal epithelial cells exposure to enterotoxigenic E. coli

Authors :
Lin, Qian
Fu, Qingqing
Su, Guoqi
Chen, Daiwen
Yu, Bing
Luo, Yuheng
Zheng, Ping
Mao, Xiangbing
Huang, Zhiqing
Yu, Jie
Luo, Junqiu
Yan, Hui
He, Jun
Source :
Brazilian Journal of Microbiology; September 2021, Vol. 52 Issue: 3 p1235-1245, 11p
Publication Year :
2021

Abstract

Bombyx morigloverin A2 (BMGlvA2) is an induced antimicrobial insect protein isolated from Bombyx mori. This study was conducted to explore the effect and potential mechanisms of BMGlvA2 on inflammatory responses and cellular functions in intestinal epithelial cells (IPEC-J2) exposure to enterotoxigenic E. coli(ETEC). IPEC-J2 cells pretreated with or without BMGlvA2 (12.5 μg/mL) were challenged by ETEC K88 (1×106CFU/well) or culture medium. We show that BMGlvA2 pretreatment increased the cell viability and improved the distribution and abundance of tight junction protein ZO-1 in IPEC-J2 cells exposure to ETEC (P< 0.05). Interestingly, BMGlvA2 not only decreased the expression levels of inflammatory cytokines such as the tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), but also decreased the expression level of Caspase3 and the apoptosis rate in the ETEC-challenged cells (P< 0.05). Importantly, BMGlvA2 decreased the protein abundances of two critical inflammation-associated signaling proteins, phosphorylated nuclear factor-kappa-B inhibitor alpha (p-IκBα) and phosphorylated nuclear factor-kappa B (p-NF-κB), in the ETEC-challenged cells. These results indicate that BMGlvA2 attenuates ETEC-induced inflammation in the IPEC-J2 cells by regulating the NF-κB signaling pathway, resulting in decreased secretion of inflammatory cytokine and reduced cell apoptosis.

Details

Language :
English
ISSN :
15178382 and 16784405
Volume :
52
Issue :
3
Database :
Supplemental Index
Journal :
Brazilian Journal of Microbiology
Publication Type :
Periodical
Accession number :
ejs56854946
Full Text :
https://doi.org/10.1007/s42770-021-00532-0