Protective Effects of <i>Lactobacillus plantarum</i> Lac16 on <i>Clostridium perfringens</i> Infection-Associated Injury in IPEC-J2 Cells

<i>Clostridium perfringens</i> (<i>C. perfringens</i>) causes intestinal injury through overgrowth and the secretion of multiple toxins, leading to diarrhea and necrotic enteritis in animals, including pigs, chickens, and sheep. This study aimed to investigate the protective...

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Auteurs principaux: Yuanhao Zhou, Baikui Wang, Qi Wang, Li Tang, Peng Zou, Zihan Zeng, Huihua Zhang, Li Gong, Weifen Li
Format: article
Langue:EN
Publié: MDPI AG 2021
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Accès en ligne:https://doaj.org/article/92448e1e2191427fa8d09d2539f7d829
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Résumé:<i>Clostridium perfringens</i> (<i>C. perfringens</i>) causes intestinal injury through overgrowth and the secretion of multiple toxins, leading to diarrhea and necrotic enteritis in animals, including pigs, chickens, and sheep. This study aimed to investigate the protective effects of <i>Lactobacillus plantarum</i> (<i>L. plantarum</i>) Lac16 on <i>C. perfringens</i> infection-associated injury in intestinal porcine epithelial cell line (IPEC-J2). The results showed that <i>L. plantarum</i> Lac16 significantly inhibited the growth of <i>C. perfringens</i>, which was accompanied by a decrease in pH levels. In addition, <i>L. plantarum</i> Lac16 significantly elevated the mRNA expression levels of host defense peptides (HDPs) in IPEC-J2 cells, decreased the adhesion of <i>C. perfringens</i> to IPEC-J2 cells, and attenuated <i>C. perfringens</i>-induced cellular cytotoxicity and intestinal barrier damage. Furthermore, <i>L. plantarum</i> Lac16 significantly suppressed <i>C. perfringens</i>-induced gene expressions of proinflammatory cytokines and pattern recognition receptors (PRRs) in IPEC-J2 cells. Moreover, <i>L. plantarum</i> Lac16 preincubation effectively inhibited the phosphorylation of p65 caused by <i>C. perfringens</i> infection. Collectively, probiotic <i>L. plantarum</i> Lac16 exerts protective effects against <i>C. perfringens</i> infection-associated injury in IPEC-J2 cells.