Scholarlink

Background <p>Decreased Aryl Hydrocarbon Receptor (AHR) signaling pathway activation is implicated in necrotizing enterocolitis (NEC) pathogenesis. <i>Limosilactobacillus reuteri</i> (<i>Lr</i>) is a probiotic that catabolizes tryptophan into AHR ligands. We have previously shown that <i>Lr</i> in its biofilm state has improved efficacy against NEC. However, the importance of the physiologic state of <i>Lr</i> (planktonic <i>vs</i>. biofilm) on AHR activation remains unknown.</p> Methods <p>In vitro experiments using intestinal epithelial cells (IEC) and in vivo experiments in premature rodents were carried out to assess the impact of planktonic- <i>vs</i>. biofilm-state <i>Lr</i> on AHR ligand production, AHR activation, and protection against NEC.</p> Results <p>Biofilm-state <i>Lr</i> was found to have increased persistence in the intestine of premature rodent pups compared to planktonic-state <i>Lr</i>. IECs exposed to conditioned media from <i>Lr</i> grown with tryptophan demonstrated increased AHR activation compared to IECs exposed to tryptophan alone. Finally, biofilm-state <i>Lr</i> was associated with increased intestinal AHR ligand production, AHR activation, and protection against NEC in rodent pups.</p> Conclusion <p>Biofilm-state <i>Lr</i> has increased persistence in the gut and protects against NEC. This protection is associated with increased AHR activation in the intestine. Through improved understanding of the interactions of <i>Lr</i> and AHR signaling, we may be able to further enhance <i>Lr</i> efficacy against NEC.</p> Impact <p><UnorderedList Mark="Bullet"> <ItemContent> <p><i>Limosilactobacillus reuteri</i> in its biofilm state increases AHR activation and reduces intestinal injury during NEC.</p> </ItemContent> <ItemContent> <p>This is the first study to look at the role of the AHR signaling pathway in <i>Limosilactobacillus reuteri</i>-mediated protection against NEC.</p> </ItemContent> <ItemContent> <p>Development of an effective therapy to prevent NEC would reduce the morbidity and mortality of this lethal disease.</p> </ItemContent> </UnorderedList></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Biofilm state Limosilactobacillus reuteri modulates aryl hydrocarbon receptor activity and suppresses experimental necrotizing enterocolitis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年8月28日

查看全文
  • Nitin Sajankila,
  • Zachary Dumbauld,
  • Yijie Wang,
  • Samantha J. Wala,
  • Mecklin V. Ragan,
  • Ameer Al-Hadidi,
  • Samuel G. Volpe,
  • Joseph Wickham,
  • Lauren Mashburn-Warren,
  • Colton Wayne,
  • Taylor Jacobs,
  • Siddharth Narayanan,
  • Michael T. Bailey,
  • Steven D. Goodman,
  • Gail E. Besner,
  • Belgacem Mihi

摘要

Background

Decreased Aryl Hydrocarbon Receptor (AHR) signaling pathway activation is implicated in necrotizing enterocolitis (NEC) pathogenesis. Limosilactobacillus reuteri (Lr) is a probiotic that catabolizes tryptophan into AHR ligands. We have previously shown that Lr in its biofilm state has improved efficacy against NEC. However, the importance of the physiologic state of Lr (planktonic vs. biofilm) on AHR activation remains unknown.

Methods

In vitro experiments using intestinal epithelial cells (IEC) and in vivo experiments in premature rodents were carried out to assess the impact of planktonic- vs. biofilm-state Lr on AHR ligand production, AHR activation, and protection against NEC.

Results

Biofilm-state Lr was found to have increased persistence in the intestine of premature rodent pups compared to planktonic-state Lr. IECs exposed to conditioned media from Lr grown with tryptophan demonstrated increased AHR activation compared to IECs exposed to tryptophan alone. Finally, biofilm-state Lr was associated with increased intestinal AHR ligand production, AHR activation, and protection against NEC in rodent pups.

Conclusion

Biofilm-state Lr has increased persistence in the gut and protects against NEC. This protection is associated with increased AHR activation in the intestine. Through improved understanding of the interactions of Lr and AHR signaling, we may be able to further enhance Lr efficacy against NEC.

Impact

Limosilactobacillus reuteri in its biofilm state increases AHR activation and reduces intestinal injury during NEC.

This is the first study to look at the role of the AHR signaling pathway in Limosilactobacillus reuteri-mediated protection against NEC.

Development of an effective therapy to prevent NEC would reduce the morbidity and mortality of this lethal disease.