Gut dysbiosis modulates hyperoxia-induced bronchopulmonary dysplasia by promoting EMT through activating TLR4/NF-κB pathway.

Yaqin Yan, Shuling Liang, Sen Li, Shunv Xie, Xiaohui Wang, Huayan Zhang

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Article in Molecular medicine (Cambridge, Mass.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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6 authors.

Yaqin YanDivision of Neonatology and Center for Newborn Care, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.

Shuling LiangDivision of Neonatology and Center for Newborn Care, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.

Sen LiGuangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, State Key Laboratory of Respiratory Disease, Guangdong Basic Research Center of Excellence for Respiratory Medicine, Guangzhou Medical University, Guangzhou, China.

Shunv XieDivision of Neonatology and Center for Newborn Care, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.

Xiaohui WangGuangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, State Key Laboratory of Respiratory Disease, Guangdong Basic Research Center of Excellence for Respiratory Medicine, Guangzhou Medical University, Guangzhou, China. xiaohuiwang2021621818@gzhmu.edu.cn.

Huayan ZhangDivision of Neonatology and Center for Newborn Care, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China. zhangh@chop.edu.

Funding

Guangzhou Health and Wellness Science and Technology Youth Talent Cultivation Project 20261A031030Guangzhou Postdoctoral Science Foundation 011302064Research foundation of Guangzhou Women and Children's Medical Center for Clinical Doctor 2024BS022

6 · The paper itself

Abstract

backgroundBronchopulmonary dysplasia (BPD) is a major cause of morbidity and mortality in premature infants. Although gut microbial dysbiosis is implicated in BPD pathogenesis, the underlying mechanisms are poorly defined. This study aims to elucidate the specific pathway through which gut dysbiosis drives BPD pathology and to identify potential therapeutic targets.

methodsThe experimental BPD model was established by hyperoxia (FiO

resultsHyperoxia exposure induced impaired alveolarization, disrupted gut barrier integrity, and gut dysbiosis. These pathological changes were accompanied by elevated pulmonary inflammation, potent activation of the TLR4/NF-κB pathway, and upregulation of epithelial-mesenchymal transition (EMT) associated markers. These changes were exacerbated by early postnatal antibiotic administration, whereas FMT from normoxic mice rescued these phenotypes, restored gut barrier function, suppressed TLR4/NF-κB signaling, and reversed EMT progression. Notably, pharmacological inhibition of TLR4 mirrored the protective effects of FMT, effectively attenuating hyperoxia-induced lung injury and EMT.

conclusionsOur findings establish a mechanistic link for the gut-lung axis in BPD, demonstrating that gut dysbiosis is a critical modulator of lung development impairment and pathological EMT via activation of the TLR4/NF-κB pathway.

Indexed as

Bronchopulmonary DysplasiaDysbiosisEpithelial-Mesenchymal TransitionGastrointestinal MicrobiomeHyperoxiaNF-kappa BSignal TransductionToll-Like Receptor 4AnimalsAnimals, NewbornDisease Models, AnimalFecal Microbiota TransplantationMaleMiceNF-kappa BTlr4 protein, mouseToll-Like Receptor 4Bronchopulmonary dysplasiaEpithelial-mesenchymal transitionFecal microbiota transplantationGut dysbiosisTLR4/NF-κB pathway

Identifiers

PMID42304226

DOI10.1186/s10020-026-01529-x

PMCPMC13508397

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.