ArticleFrontiers in immunology2022
Selective targeting of MD2 attenuates intestinal inflammation and prevents neonatal necrotizing enterocolitis by suppressing TLR4 signaling.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- From homeostasis to dysregulation: human milk, microbial metabolites, and the preterm intestinal microenvironment in necrotizing enterocolitis.Translational pediatrics · 2026Review
- Integrated multi-omics analysis reveals dendritic cell centered regulatory networks and therapeutic targets in necrotizing enterocolitis.Frontiers in immunology · 2026Article
- Review
- 1-methylnicotinamide attenuated inflammation and regulated flora in Necrotizing enterocolitis.PloS one · 2025Article
- The Galloyl Group Enhances the Inhibitory Activity of Catechins against LPS-Triggered Inflammation in RAW264.7 Cells.Foods (Basel, Switzerland) · 2024Article
- Immunological aspects of necrotizing enterocolitis models: a review.Frontiers in immunology · 2024Review
- New insights into intestinal macrophages in necrotizing enterocolitis: the multi-functional role and promising therapeutic application.Frontiers in immunology · 2023Review
- The Emerging Roles of Ferroptosis in Neonatal Diseases.Journal of inflammation research · 2023Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neonatal necrotizing enterocolitis (NEC) is an inflammatory disease that occurs in premature infants and has a high mortality rate; however, the mechanisms behind this disease remain unclear. The TLR4 signaling pathway in intestinal epithelial cells, mediated by TLR4, is important for the activation of the inflammatory storm in NEC infants. Myeloid differentiation protein 2 (MD2) is a key auxiliary component of the TLR4 signaling pathway. In this study, MD2 was found to be significantly increased in intestinal tissues of NEC patients at the acute stage. We further confirmed that MD2 was upregulated in NEC rats. MD2 inhibitor (MI) pretreatment reduced the occurrence and severity of NEC in neonatal rats, inhibited the activation of NF-κB and the release of inflammatory molecules (TNF-α and IL-6), and reduced the severity of intestinal injury. MI pretreatment significantly reduced enterocyte apoptosis while also maintaining tight junction proteins, including occludin and claudin-1, and protecting intestinal mucosal permeability in NEC rats. In addition, an NEC
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