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<p>Porcine β-defensin 2 (pBD2) is an antimicrobial peptide with both antibacterial and immunomodulatory activities and plays an important role against pathogens. Our previous results suggested that pBD2 might exert its protective effects against <i>E. coli</i> by regulating cell apoptosis and proliferation through the Akt signaling pathway. However, the specific roles and underlying mechanisms of pBD2 in regulating these cellular processes remain unclear. In this study, porcine intestinal epithelial cells (IPEC-J2) were treated with pBD2 in the presence of Enterotoxigenic <i>E. coli</i> (ETEC) K88 challenge. pBD2 inhibited ETEC-induced apoptosis, decreased the levels of cleaved caspase-3 and caspase-9, and restored mitochondrial membrane potential, suggesting that pBD2 inhibited ETEC-induced apoptosis <i>via</i> the intrinsic apoptotic pathway. Moreover, pBD2 restored cell proliferation and attenuated ETEC-induced cell cycle arrest in the G0/G1 phase, and upregulated the expression of proliferation-related genes including <i>CDC25A</i>, <i>CDC6</i>, <i>E2F2</i> and <i>PCNA</i>. In addition, the results further revealed that pBD2 attenuated cell apoptosis and restored cell proliferation in ETEC K88-infected IPEC-J2 cells by inhibiting the Akt signaling pathway. Our results provide further evidence for the protective effects of pBD2 on intestinal epithelial cells and extend its known biological roles. This study elucidates an anti-apoptotic and pro-proliferative mechanism of pBD2 against ETEC infection and provides insights into its potential application.</p>

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Porcine Beta Defensin 2 Alleviates Apoptosis and Restores Proliferation in IPEC-J2 Cells Challenged with ETEC K88 by Inhibiting the Akt Signaling Pathway

  • 期刊论文

  • 发表日期：

    2026年7月7日

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  • Guixin Zhu,
  • Mingke Gu,
  • Qingbo Zhao,
  • Zhilong Du,
  • Kejun Wang,
  • Chunli Li

摘要

Porcine β-defensin 2 (pBD2) is an antimicrobial peptide with both antibacterial and immunomodulatory activities and plays an important role against pathogens. Our previous results suggested that pBD2 might exert its protective effects against E. coli by regulating cell apoptosis and proliferation through the Akt signaling pathway. However, the specific roles and underlying mechanisms of pBD2 in regulating these cellular processes remain unclear. In this study, porcine intestinal epithelial cells (IPEC-J2) were treated with pBD2 in the presence of Enterotoxigenic E. coli (ETEC) K88 challenge. pBD2 inhibited ETEC-induced apoptosis, decreased the levels of cleaved caspase-3 and caspase-9, and restored mitochondrial membrane potential, suggesting that pBD2 inhibited ETEC-induced apoptosis via the intrinsic apoptotic pathway. Moreover, pBD2 restored cell proliferation and attenuated ETEC-induced cell cycle arrest in the G0/G1 phase, and upregulated the expression of proliferation-related genes including CDC25A, CDC6, E2F2 and PCNA. In addition, the results further revealed that pBD2 attenuated cell apoptosis and restored cell proliferation in ETEC K88-infected IPEC-J2 cells by inhibiting the Akt signaling pathway. Our results provide further evidence for the protective effects of pBD2 on intestinal epithelial cells and extend its known biological roles. This study elucidates an anti-apoptotic and pro-proliferative mechanism of pBD2 against ETEC infection and provides insights into its potential application.