Figure 3.

Mechanical stretch causes inflammatory responses associated with release of mediators that can worsen lung injury leading to “biotrauma.” Mechanical stretch of alveoli results in increased expression of small fragment hyaluronan (sHA) and activation of cytoplasmic proline-rich tyrosine kinase- 2 (PyK2); polymorphonuclear leukocyte (PMN) infiltration that release soluble mediators such as cytokines and platelet-derived growth factor (PDGF); increased production of extracellular matrix (ECM) proteins including transforming growth factor- β1 (TGF-β1), collagen, elastin, fibronectin laminin, lumican, proteoglycan, and glycosaminoglycans.

During the exudative phase of acute respiratory distress syndrome, the influx of T regulatory cells (Treg) may play a critical role in the crosstalk between innate and adaptive immune systems that normally would modulate the transition from injury to repair in resolving lung injury. ATI = alveolar type I; ATII = alveolar type II.