期刊
FOOD & FUNCTION
卷 12, 期 13, 页码 5821-5836出版社
ROYAL SOC CHEMISTRY
DOI: 10.1039/d1fo00269d
关键词
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资金
- National Natural Science Foundation of China [32030101, 31872368, 31672434]
- China Agriculture Research System [CARS-35]
- Natural Science Foundation of Heilongjiang Province [TD2019C001]
The study demonstrates that l-threonine can effectively increase the expression of beta-defensins and reduce inflammatory cytokines in porcine intestinal epithelial cells. Furthermore, l-threonine helps alleviate LPS-induced intestinal mucosal barrier damage, suggesting its potential as a promising approach to enhance disease resistance and intestinal health in animals.
The use of antimicrobial peptide (AMP), found in all forms of life and playing a pivotal role in the innate immune system, has been developed as a new strategy for maintaining intestinal health and reducing antibiotic usage due to its ability to resist pathogens and commensal microbes. The current study investigated the effects of l-threonine on beta-defensin expression, the intestinal mucosal barrier and inflammatory cytokine expression in porcine intestinal epithelial cell lines (IPEC-J2). The results revealed that in IPEC-J2 cells, l-threonine significantly increased the expression of beta-defensin (including pBD-1, pBD-2, and pBD-3) in a dose- and time-dependent manner (P < 0.05). By using different concentrations and treatment times of l-threonine, the results showed that the expression of beta-defensin was upregulated to the greatest extent in IPEC-J2 cells cultured with 1 mM l-threonine for 24 h. Although the mRNA expression levels of beta-defensins were markedly increased (P < 0.05), there was relatively little inducible pBD-1, pBD-2 and pBD-3 mRNA expression at the sub-confluent and confluent densities in comparison with post-confluent densities. Furthermore, we found that l-threonine enhanced the beta-defensin expression by suppressing the expression of SIRT1, which increased acetylated p65 expression, and activating the NF-kappa B signaling pathway, which induced the translocation of p65 from the cytoplasm to the nucleus. In addition, l-threonine significantly prevented LPS-induced intestinal mucosal barrier damage by attenuating the decreasing tendency of the mRNA expression of Mucin1 and Mucin2 (P < 0.05). Simultaneously, l-threonine enhanced the expression of beta-defensins upon LPS challenge in IPEC-J2 cells (P < 0.05). l-Threonine obviously decreased the mRNA expression of inflammatory cytokines compared to that in untreated cells (P < 0.05). In conclusion, l-threonine can upregulate beta-defensin expression and reduce inflammatory cytokine expression in IPEC-J2 cells; meanwhile, l-threonine alleviates LPS-induced intestinal mucosal barrier damage in porcine intestinal epithelial cells. The l-threonine-mediated modulation of endogenous defensin expression may be a promising approach to reduce antibiotic use, enhance disease resistance and intestinal health in animals.
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