Related Experiment Video
Updated: Aug 30, 2025
A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
Role of Mitophagy-based TLR9 Signal Pathway in Neonatal Ventilator-induced Lung Injury
Jinni Chen1, Dawei Li2, Zhenzhen Huang1
1Department of Respiratory, Hainan Maternal and Children's Medical Center, Haikou, 570206, China. yongzihan6921586@163.com.
Abstract:
The study focused on the role of mitophagy in neonatal ventilator-induced lung injury (VILI). Immunoassays were used to study the TLR9 signaling pathway of neonatal VILI, expected to provide a feasible solution for neonatal VILI. The mice were randomly divided into four groups, group A: spontaneous breathing group; group B: normal tidal volume (VT) group (VT=9mL/kg); group C: high VT group (VT=39mL/kg); and group D: ODN2088 (400μg/ Only) intervention + high VT group. The four groups were compared for the expression of inflammatory factors. It was found that as the culture time increased, the expression of TLR9, MyD88, and NF-κBp65 in the lung tissue of the large VT group was significantly higher than those in the spontaneous breathing group and normal VT group, and the differences were statistically significant; and TLR9 inhibitors could activate the TLR9-MyD88 signaling pathway to up-regulate the expression of NF-κB, mediating the release of inflammatory factors to cause VILI.
Insights
Neonatal ventilator-induced lung injury (VILI) involves the TLR9-MyD88 pathway. Inhibiting TLR9 may offer a therapeutic strategy for VILI by modulating inflammatory responses in neonatal lungs.
Area of Science:
- Neonatology
- Pulmonology
- Immunology
Background:
- Neonatal ventilator-induced lung injury (VILI) is a significant clinical concern.
- Mitophagy and the TLR9 signaling pathway are implicated in VILI pathogenesis.
Purpose of the Study:
- To investigate the role of the TLR9 signaling pathway in neonatal VILI.
- To explore potential therapeutic interventions for VILI.
Main Methods:
- Neonatal mice were divided into four groups: spontaneous breathing, normal tidal volume (VT), high VT, and high VT with TLR9 inhibitor (ODN2088).
- Immunoassays were used to measure the expression of TLR9, MyD88, and NF-κBp65 in lung tissue.
- Inflammatory factor expression was compared across groups.
Main Results:
- High VT significantly increased TLR9, MyD88, and NF-κBp65 expression in neonatal lung tissue compared to spontaneous breathing and normal VT groups.
- TLR9 inhibitors activated the TLR9-MyD88 pathway, up-regulating NF-κB.
- This activation mediated inflammatory factor release, contributing to VILI.
Conclusions:
- The TLR9-MyD88-NF-κB signaling pathway plays a crucial role in mediating neonatal VILI.
- Targeting TLR9 may represent a viable therapeutic strategy for preventing or treating VILI in neonates.
