Abstract
Acute respiratory distress syndrome (ARDS) is a clinical syndrome associated with oxygenation failure resulting from a direct pulmonary or indirect systemic insult. It is a complex etiological phenomenon involving an array of immune cells acting in a delicate balance between pathogen clearance and immunopathology. There is emerging evidence of the involvement of different immune cell types in ARDS pathogenesis. This includes polarization of alveolar macrophages (AMs), neutrophil netosis, the pro-inflammatory response of T helper 17 subsets, and the anti-inflammatory and regenerative role of T regulatory cell subsets. Knowledge of these pathogenic mechanisms has led to translational opportunities, for example, research in the use of methylprednisolone, DNAse, aspirin, keratinocyte growth factor and in the development of stem cell therapy for ARDS. Discovering subgroups of patients with ARDS afflicted with homogenous pathologic mechanisms can provide prognostic and/or predictive insight that will enable precision medicine. Lastly, new high dimensional immunomic technologies are promising tools in evaluating the host immune response in ARDS and will be discussed in this review.