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Background <p>Human breast milk-derived exosomes have been shown to prevent necrotizing enterocolitis (NEC). However, the mechanism remains unclear. This study aims to examine the role of miR-144-5p in repairing the damage of the tight junction barrier caused by NEC and its underlying mechanism.</p> Methods <p>Differentially expressed exosome-derived miRNAs from term and preterm breast milk were identified through miRNA sequencing. Subsequently, the biological role and mechanism of the miRNA were studied both in vitro and in vivo.</p> Results <p>We found that exosomal miR-144-5p enhances the viability of intestinal epithelial cells in vitro and increases claudin-1 protein levels in vivo; Overexpressed miR-144-5p decreases interleukin-1beta (IL-1β) protein levels both in vitro and in vivo. Mechanistically, miR-144-5p alleviates intestinal inflammation and improves epithelial barrier function by downregulating toll-like receptor 4 (TLR4) expression and inhibiting the NF-κB signaling pathway.</p> Conclusions <p>Exosomal miR-144-5p protects against experimental NEC by inhibiting the TLR4/NF-κB signaling pathway. This study reveals a previously unknown regulatory mechanism in the progression of NEC.</p> Impact <p><UnorderedList Mark="Bullet"> <ItemContent> <p>Overexpression of miR-144-5p significantly decreases TLR4 expression, thereby inhibiting the TLR4 signaling pathway.</p> </ItemContent> <ItemContent> <p>MiR-144-5p reduces the production of inflammatory cytokines and prevents disruption of the tight junction protein claudin-1.</p> </ItemContent> <ItemContent> <p>This study is the first to confirm that human milk exosome miRNAs protect tight junctions from LPS-induced damage by modulating the TLR4/NF-κB signaling pathway.</p> </ItemContent> <ItemContent> <p>It offers a new perspective on understanding the pathogenesis of NEC.</p> </ItemContent> <ItemContent> <p>It expands the therapeutic options for necrotizing enterocolitis.</p> </ItemContent> </UnorderedList></p>

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Human milk exosomal-miR-144-5p alleviates neonatal necrotizing enterocolitis by regulating the TLR4/NF-κB pathway

  • 期刊论文

  • 发表日期：

    2026年7月29日

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  • Zhenjiang Chen,
  • Chengchao Chen,
  • Xiaohan Hu,
  • Fang Guo,
  • Qilin Luo,
  • Haitao Lv,
  • Xueping Zhu

摘要

Background

Human breast milk-derived exosomes have been shown to prevent necrotizing enterocolitis (NEC). However, the mechanism remains unclear. This study aims to examine the role of miR-144-5p in repairing the damage of the tight junction barrier caused by NEC and its underlying mechanism.

Methods

Differentially expressed exosome-derived miRNAs from term and preterm breast milk were identified through miRNA sequencing. Subsequently, the biological role and mechanism of the miRNA were studied both in vitro and in vivo.

Results

We found that exosomal miR-144-5p enhances the viability of intestinal epithelial cells in vitro and increases claudin-1 protein levels in vivo; Overexpressed miR-144-5p decreases interleukin-1beta (IL-1β) protein levels both in vitro and in vivo. Mechanistically, miR-144-5p alleviates intestinal inflammation and improves epithelial barrier function by downregulating toll-like receptor 4 (TLR4) expression and inhibiting the NF-κB signaling pathway.

Conclusions

Exosomal miR-144-5p protects against experimental NEC by inhibiting the TLR4/NF-κB signaling pathway. This study reveals a previously unknown regulatory mechanism in the progression of NEC.

Impact

Overexpression of miR-144-5p significantly decreases TLR4 expression, thereby inhibiting the TLR4 signaling pathway.

MiR-144-5p reduces the production of inflammatory cytokines and prevents disruption of the tight junction protein claudin-1.

This study is the first to confirm that human milk exosome miRNAs protect tight junctions from LPS-induced damage by modulating the TLR4/NF-κB signaling pathway.

It offers a new perspective on understanding the pathogenesis of NEC.

It expands the therapeutic options for necrotizing enterocolitis.