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Presentation date

Summer 8-12-2021

College, Institute, or Department

Surgery

Faculty Mentor

Keely L. Buesing MD

Research Mentor

Hannah R. Weber MFS, Premila D. Leiphrakpam PhD

Abstract

Acute respiratory distress syndrome (ARDS) is a lethal disease condition in critically ill patients with a reported mortality rate reaching 45%. The current treatment modalities available for severe ARDS are invasive and carry significant risk for patients. Most published studies involving smoke inhalation utilize another simultaneous injury (such as cutaneous burn) to increase pathology burden of their animal models. This introduces confounding variables to investigations which aim to concentrate on inhalation injury. In this study, we evaluated the potential molecular targets associated with isolated smoke inhalation-induced ARDS.

We observed an increase in lung injury score and wet/dry ratio 48h post smoke inhalation together with upregulation of inflammatory markers, IL-1βand IL-6 levels. Furthermore, there was a decrease in phosphorylation of cell survival marker Akt and an increase in pro-apoptotic protein BAX at 48h post smoke inhalation. These results indicate that smoke inhalation induced inflammatory processes resulting in increased apoptosis and decreased cell survival in lung parenchymal cells. Use of this unique model may be of benefit in studying the pathophysiology of inhalation injury and for the development of novel therapeutic strategies.

Keywords

smoke inhalation, ARDS, lung injury, acute respiratory distress syndrome

Cell death mechanism in an isolated wood smoke inhalation induced-ARDS large animal model

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