ArticleBMC microbiology2025
Inhibition of Enterotoxigenic Escherichia coli adhesion via aptamers prevents infection in IPEC-J2 cells.
Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Isolation, Characterization, and Anti-Inflammatory Effects ofFoods (Basel, Switzerland) · 2026Article
- Antibacterial Immunotherapy: Mechanistic Insights, Emerging Therapeutic Strategies, and Clinical Translation.Infection and drug resistance · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
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.
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Registered trials
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