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Objective <p>This study aims to investigate the role of TREM1 in necrotizing enterocolitis (NEC).</p> Methods <p>A mouse model of NEC was established through artificial feeding combined with hypoxia-cold stress. Intestinal injury was assessed via H&amp;E staining. Inflammatory cytokines were measured by ELISA, and reactive oxygen species (ROS) activity was evaluated using DHE staining. Intestinal permeability was determined by the fluorescein-isothiocyanate-dextran (FITC-dextran) method. Tight junction proteins were analyzed through immunohistochemistry and western blotting. The expression of CD86 and CD206 in M1 and M2 macrophages was assessed by immunofluorescence, and the mRNA levels of M1 and M2 markers (CD86, iNOS, CD206, and Arg-1) were detected by RT-qPCR. Proteins involved in ER stress were analyzed using western blotting.</p> Results <p>Inhibition of TREM1 was found to reduce intestinal injury, inflammation, and oxidative stress, improve intestinal barrier function, suppress M1 macrophage polarization, and attenuate ER stress in NEC mice. Moreover, we found that treatment with the ER stress inducer tunicamycin reversed these protective effects of TREM1 inhibition.</p> Conclusion <p>TREM1 inhibition protects against intestinal injury, inflammation, oxidative stress, intestinal barrier damage, and M1 macrophage polarization in NEC mice by suppressing ER stress.</p>

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Targeting TREM1 Ameliorates Necrotizing Enterocolitis in Neonatal Mice by Inhibiting Endoplasmic Reticulum Stress and Regulating Macrophage Polarization

  • 期刊论文

  • 发表日期：

    2025年6月24日

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  • Xiaolei Xie,
  • Binbin Qiu,
  • Jin Huang

摘要

Objective

This study aims to investigate the role of TREM1 in necrotizing enterocolitis (NEC).

Methods

A mouse model of NEC was established through artificial feeding combined with hypoxia-cold stress. Intestinal injury was assessed via H&E staining. Inflammatory cytokines were measured by ELISA, and reactive oxygen species (ROS) activity was evaluated using DHE staining. Intestinal permeability was determined by the fluorescein-isothiocyanate-dextran (FITC-dextran) method. Tight junction proteins were analyzed through immunohistochemistry and western blotting. The expression of CD86 and CD206 in M1 and M2 macrophages was assessed by immunofluorescence, and the mRNA levels of M1 and M2 markers (CD86, iNOS, CD206, and Arg-1) were detected by RT-qPCR. Proteins involved in ER stress were analyzed using western blotting.

Results

Inhibition of TREM1 was found to reduce intestinal injury, inflammation, and oxidative stress, improve intestinal barrier function, suppress M1 macrophage polarization, and attenuate ER stress in NEC mice. Moreover, we found that treatment with the ER stress inducer tunicamycin reversed these protective effects of TREM1 inhibition.

Conclusion

TREM1 inhibition protects against intestinal injury, inflammation, oxidative stress, intestinal barrier damage, and M1 macrophage polarization in NEC mice by suppressing ER stress.