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Updated: Dec 30, 2025

Refined Murine Model of Idiopathic Pulmonary Fibrosis
Published on: June 17, 2025
Fibroblast growth factor 10 alleviates particulate matter-induced lung injury by inhibiting the HMGB1-TLR4 pathway
Lingjing Liu1, Chenjian Song2, Jingli Li1
1Department of Pulmonary Medicine, Wenzhou Medical University First Affiliated Hospital, Wenzhou 325006, China.
Abstract:
Exposure to particulate matter (PM) is associated with increased incidence of respiratory diseases. The present study aimed to investigate the roles of fibroblast growth factor 10 (FGF10) in PM-induced lung injury. Mice were intratracheally instilled with FGF10 or phosphate-buffered saline at one hour before instillation of PM for two consecutive days. In addition, the anti-inflammatory impact of FGF10 in vitro and its effect on the high-mobility group box 1 (HMGB1)-toll-like receptor 4 (TLR4) pathway was investigated. It was found that PM exposure is associated with increased inflammatory cell infiltration into the lung and increased vascular protein leakage, while FGF10 pretreatment attenuated both of these effects. FGF10 also decreased the PM-induced expression of interleukin (IL)-6, IL-8, tumor necrosis factor-α and HMGB1 in murine bronchoalveolar lavage fluid and in the supernatants of human bronchial epithelial cells exposed to PM. FGF10 exerted anti-inflammatory and cytoprotective effects by inhibiting the HMGB1-TLR4 pathway. These results indicate that FGF10 may have therapeutic values for PM-induced lung injury.
Insights
Fibroblast growth factor 10 (FGF10) protects against particulate matter (PM) lung injury by reducing inflammation and cell damage. FGF10 may offer a therapeutic strategy for PM-induced respiratory diseases.
Area of Science:
- Environmental Health
- Pulmonary Medicine
- Molecular Biology
Background:
- Particulate matter (PM) exposure is a significant risk factor for respiratory diseases.
- The precise mechanisms underlying PM-induced lung injury require further elucidation.
- Fibroblast growth factor 10 (FGF10) role in PM-induced lung injury is not well understood.
Purpose of the Study:
- To investigate the protective effects of FGF10 against PM-induced lung injury.
- To explore the anti-inflammatory impact of FGF10 in vitro.
- To determine FGF10's effect on the high-mobility group box 1 (HMGB1)-toll-like receptor 4 (TLR4) pathway.
Main Methods:
- Mice were pretreated with FGF10 or saline before PM exposure.
- Inflammatory cell infiltration and vascular protein leakage were assessed.
- Expression of inflammatory cytokines (IL-6, IL-8, TNF-α) and HMGB1 was measured.
- In vitro studies assessed FGF10's anti-inflammatory effects on human bronchial epithelial cells exposed to PM.
Main Results:
- FGF10 pretreatment significantly reduced inflammatory cell infiltration and vascular protein leakage in PM-exposed mice.
- FGF10 decreased the expression of IL-6, IL-8, TNF-α, and HMGB1 induced by PM.
- FGF10 demonstrated anti-inflammatory and cytoprotective effects by inhibiting the HMGB1-TLR4 pathway.
Conclusions:
- FGF10 exhibits significant protective effects against PM-induced lung injury.
- FGF10 alleviates PM-induced inflammation and cellular damage.
- FGF10 may represent a potential therapeutic agent for treating PM-induced lung injury.

