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Related Experiment Video

Updated: May 18, 2026

Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
11:07

Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation

Published on: July 6, 2019

Altered lung function relates to inflammation in an acute LPS mouse model.

Hanna Falk Håkansson1, Amir Smailagic, Charlott Brunmark

  • 1Former employees of AstraZeneca R&D, Lund, Sweden. Hanna_fn@bredband.net

Pulmonary Pharmacology & Therapeutics
|September 15, 2012
PubMed
Summary

Acute lung injury from lipopolysaccharide (LPS) causes inflammation and impaired lung function in mice. This study reveals a direct temporal link between peak inflammation and lung dysfunction, highlighting inflammation’s causative role in respiratory diseases.

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Non-Invasive Endotracheal Administration of Lipopolysaccharide to Induce Acute Lung Injury in Rodents

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Area of Science:

  • Pulmonary Medicine
  • Toxicology
  • Immunology

Background:

  • Preclinical models using lipopolysaccharide (LPS) are vital for studying acute lung injury (ALI) and its relevance to chronic obstructive pulmonary disease (COPD).
  • While LPS-induced lung inflammation is understood, its temporal relationship with specific lung function changes remains unclear.

Purpose of the Study:

  • To investigate the temporal dynamics of LPS-induced lung inflammation and its correlation with lung function alterations in a mouse model.
  • To evaluate the efficacy of budesonide in mitigating LPS-induced lung inflammation and dysfunction.

Main Methods:

  • Mice were exposed to acute LPS inhalation, with assessments up to 96 hours post-exposure.
  • Quantified inflammatory cells and mediators in bronchoalveolar lavage fluid (BALF).
  • Measured non-invasive and invasive lung function parameters at corresponding time points. Evaluated budesonide's inhibitory effects.

Main Results:

  • LPS inhalation induced histopathological changes and peak inflammatory cell infiltration at 48 hours.
  • Significantly elevated inflammatory mediators and altered lung capacity and mechanics were observed at 48 hours.
  • Oral budesonide administration effectively prevented LPS-induced lung inflammation and dysfunction.

Conclusions:

  • A clear temporal relationship exists between peak inflammatory cell influx and significant lung function impairment following LPS exposure.
  • These findings suggest a causative role for inflammation in the functional consequences of ALI.
  • This study enhances understanding of lung inflammation's impact on respiratory diseases.