Mouse Model of Oleic Acid-Induced Acute Respiratory Distress Syndrome.

J Vis Exp

Laboratório de Imunofarmacologia, Fundação Oswaldo Cruz, FIOCRUZ; Laboratório de Imunofarmacologia, Departamento de Bioquímica, Instituto Biomédico, Universidade Federal do Estado do Rio de Janeiro; Programa de Pós-Graduação em Biologia Molecular e Celular, Universidade Federal do Estado do Rio de Janeiro; Programa de Pós-Graduação em Ciências e Biotecnologia, Universidade Federal Fluminense; Programa de Pós-Graduação em Neurociências, Universidade Federal Fluminense;

Published: June 2022

Acute respiratory distress syndrome (ARDS) is a significant threat to critically ill patients with a high fatality rate. Pollutant exposure, cigarette smoke, infectious agents, and fatty acids can induce ARDS. Animal models can mimic the complex pathomechanism of the ARDS. However, each of them has limitations. Notably, oleic acid (OA) is increased in critically ill patients with harmful effects on the lung. OA can induce lung injury by emboli, disrupting tissue, altering pH, and impairing edema clearance. OA-induced lung injury model resembles various features of ARDS with endothelial injury, increased alveolar permeability, inflammation, membrane hyaline formation, and cell death. Herein, induction of lung injury is described by injecting OA (in salt form) directly into the lung and intravenously in a mouse since it is the physiological form of OA at pH 7. Thus, the injection of OA in the salt form is a helpful animal model to study lung injury/ARDS without causing emboli or altering the pH, thereby getting close to what is happening in critically ill patients.

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Source
http://dx.doi.org/10.3791/63566DOI Listing

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