Related Experiment Video
Updated: May 1, 2026
Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Maresin 1 mitigates LPS-induced acute lung injury in mice
Jie Gong1, Zhou-yang Wu, Hong Qi
1Department of Critical Care Medicine, Institute of Anesthesia and Critical Care, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Background And Purpose:
Acute lung injury (ALI) is a severe illness with a high rate of mortality. Maresin 1 (MaR1) was recently reported to regulate inflammatory responses. We used a LPS-induced ALI model to determine whether MaR1 can mitigate lung injury.
Experimental Approach:
Male BALB/c mice were injected, intratracheally, with either LPS (3 mg·kg(-1) ) or normal saline (1.5 mL·kg(-1) ). After this, normal saline, a low dose of MaR1 (0.1 ng per mouse) or a high dose of MaR1 (1 ng per mouse) was given i.v. Lung injury was evaluated by detecting arterial blood gas, pathohistological examination, pulmonary oedema, inflammatory cell infiltration, inflammatory cytokines in the bronchoalveolar lavage fluid and neutrophil-platelet interactions.
Key Results:
The high dose of MaR1 significantly inhibited LPS-induced ALI by restoring oxygenation, attenuating pulmonary oedema and mitigating pathohistological changes. A combination of elisa and immunohistochemistry showed that high-dose MaR1 attenuated LPS-induced increases in pro-inflammatory cytokines (TNF-α, IL-1β and IL-6), chemokines [keratinocyte chemokine, monocyte chemoattractant protein-5, macrophage inflammatory protein (MIP)-1α and MIP-1γ], pulmonary myeloperoxidase activity and neutrophil infiltration in the lung tissues. Consistent with these observations, flow cytometry and Western blotting indicated that MaR1 down-regulated LPS-induced neutrophil adhesions and suppressed the expression of intercellular adhesion molecule (ICAM)-1, P-selection and CD24.
Conclusions And Implications:
High-dose MaR1 mitigated LPS-induced lung injury in mice by inhibiting neutrophil adhesions and decreasing the levels of pro-inflammatory cytokines.
Insights
Maresin 1 (MaR1) significantly reduced lung injury in mice by decreasing inflammatory cytokines and neutrophil adhesion. This finding offers potential therapeutic avenues for acute lung injury (ALI).
Area of Science:
- Pulmonary Medicine
- Inflammation Research
- Biomedical Science
Background:
- Acute lung injury (ALI) is a critical condition with high mortality rates.
- Maresin 1 (MaR1) is recognized for its role in modulating inflammatory processes.
- Investigating MaR1's potential to counteract ALI is crucial for developing new treatments.
Purpose of the Study:
- To evaluate the efficacy of Maresin 1 (MaR1) in mitigating lipopolysaccharide (LPS)-induced acute lung injury (ALI) in a murine model.
- To determine the dose-dependent effects of MaR1 on ALI pathophysiology.
- To elucidate the molecular mechanisms underlying MaR1's protective effects in ALI.
Main Methods:
- Establishment of an LPS-induced ALI model in male BALB/c mice.
- Intravenous administration of varying doses of MaR1 (0.1 ng or 1 ng per mouse) or saline.
- Comprehensive assessment of lung injury, including blood gas analysis, histopathology, edema measurement, inflammatory cell counts, cytokine profiling, and neutrophil-platelet interactions.
Main Results:
- High-dose MaR1 administration significantly ameliorated ALI symptoms, improving oxygenation and reducing pulmonary edema and tissue damage.
- MaR1 suppressed LPS-induced elevations in pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and chemokines.
- MaR1 inhibited neutrophil infiltration and adhesion by down-regulating ICAM-1, P-selectin, and CD24 expression.
Conclusions:
- High-dose Maresin 1 (MaR1) demonstrates significant therapeutic potential in reducing acute lung injury (ALI) severity.
- MaR1 effectively mitigates lung inflammation by inhibiting neutrophil adhesion and suppressing pro-inflammatory cytokine production.
- These findings highlight MaR1 as a promising candidate for the treatment of ALI.
