L-Threonine upregulates the expression of β-defensins by activating the NF-κB signaling pathway and suppressing SIRT1 expression in porcine intestinal epithelial cells

Food Funct. 2021 Jul 5;12(13):5821-5836. doi: 10.1039/d1fo00269d.

Abstract

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 β-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 β-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 β-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 β-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 β-defensin expression by suppressing the expression of SIRT1, which increased acetylated p65 expression, and activating the NF-κB 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 β-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 β-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.

MeSH terms

  • Animals
  • Cell Line
  • Cytokines / genetics
  • Cytokines / metabolism
  • Epithelial Cells / drug effects*
  • Gene Expression Regulation / drug effects
  • Intestinal Mucosa / metabolism
  • Intestines / drug effects*
  • NF-kappa B / genetics
  • NF-kappa B / metabolism*
  • Neoplasm Proteins
  • Nucleocytoplasmic Transport Proteins
  • RNA, Messenger / metabolism
  • Signal Transduction / drug effects*
  • Sirtuin 1 / genetics
  • Sirtuin 1 / metabolism*
  • Swine
  • Threonine / metabolism
  • Threonine / pharmacology*
  • Up-Regulation / drug effects*
  • beta-Defensins / genetics
  • beta-Defensins / metabolism*

Substances

  • Cytokines
  • NF-kappa B
  • Neoplasm Proteins
  • Nucleocytoplasmic Transport Proteins
  • RNA, Messenger
  • beta-Defensins
  • Threonine
  • Sirtuin 1