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<p><i>Enterotoxigenic Escherichia coli</i> (ETEC) is a well-known strain associated with post-weaning diarrhea. Consequently, strategies to prevent and inhibit ETEC infections are critically important. Aptamers are single-stranded DNA or RNA sequences that exhibit high affinity and specificity for binding to target molecules. In this study, we used the intestinal porcine epithelial cell line IPEC-J2 as an in vitro model to demonstrate that two aptamers, K88-Apt A04 (a fimbrial-specific aptamer targeting ETEC K88) and K88-Apt 37 (a cell-specific aptamer targeting ETEC K88) effectively inhibited the adhesion of ETEC K88 to intestinal epithelial cells. We established an ETEC K88-IPEC-J2 interaction model by exposing the IPEC-J2 cell line to ETEC K88 at a multiplicity of infection of 10. Our findings revealed that the aptamers inhibited ETEC K88 adhesion to IPEC-J2 cells in a concentration-dependent manner, primarily through adherence inhibition and prevention. Furthermore, enzyme-linked immunosorbent assay and mRNA expression analyses indicated that the aptamers reduced the secretion of pro-inflammatory cytokines triggered by ETEC K88 infection. In conclusion the aptamers demonstrated the ability to reduce ETEC K88-induced cytotoxicity in IPEC-J2 cells in vitro.</p>

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Inhibition of Enterotoxigenic Escherichia coli adhesion via aptamers prevents infection in IPEC-J2 cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月25日

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  • Zefeng Wang,
  • Tao Xu,
  • Jianxi Tan,
  • Yan Zhou,
  • Qiyi Li,
  • Zhihui Peng

摘要

Enterotoxigenic Escherichia coli (ETEC) is a well-known strain associated with post-weaning diarrhea. Consequently, strategies to prevent and inhibit ETEC infections are critically important. Aptamers are single-stranded DNA or RNA sequences that exhibit high affinity and specificity for binding to target molecules. In this study, we used the intestinal porcine epithelial cell line IPEC-J2 as an in vitro model to demonstrate that two aptamers, K88-Apt A04 (a fimbrial-specific aptamer targeting ETEC K88) and K88-Apt 37 (a cell-specific aptamer targeting ETEC K88) effectively inhibited the adhesion of ETEC K88 to intestinal epithelial cells. We established an ETEC K88-IPEC-J2 interaction model by exposing the IPEC-J2 cell line to ETEC K88 at a multiplicity of infection of 10. Our findings revealed that the aptamers inhibited ETEC K88 adhesion to IPEC-J2 cells in a concentration-dependent manner, primarily through adherence inhibition and prevention. Furthermore, enzyme-linked immunosorbent assay and mRNA expression analyses indicated that the aptamers reduced the secretion of pro-inflammatory cytokines triggered by ETEC K88 infection. In conclusion the aptamers demonstrated the ability to reduce ETEC K88-induced cytotoxicity in IPEC-J2 cells in vitro.