Washington University in St. Louis (WU)
Acute lung injury develops as an insult precipitates alveolar injury, endothelial damage, and increased vascular permeability that when paired with dysregulated inflammatory signaling and alveolar remodeling, often results in critical illness with substantial morbidity and mortality. The mechanism by which resident cells within the lung microenvironment communicate and influence the recruitment and activation of inflammatory cells and dysregulated alveolar remodeling remains incompletely understood and existing data is primarily derived from non-human model systems or derived from peripheral blood markers of inflammation in humans. We propose that distinct signatures of cell-to-cell communication driving inflammation and matrix remodeling within the alveolar microenvironment are a determinant of the subtype, degree, and trajectory of acute lung injury. We aim to define these in the context of cellular and tissue specific programming that occurs during acute injury within the lung.