What do we know about mechanical strain in lung alveoli?

Abstract

The pulmonary alveolus, terminal gas-exchange unit of the lung, is composed of alveolar epithelial and endothelial cells separated by a thin basement membrane and interstitial space. These cells participate in the maintenance of a delicate system regulated not only by biological factors but also by the mechanical environment of the lung, which undergoes dynamic deformation during breathing. Clinical and animal studies as well as cell culture studies point toward a strong influence of mechanical forces on lung cells and tissues including effects on growth and repair, surfactant release, injury, and inflammation. However, despite substantial advances in our understanding of lung mechanics over the last half century, there are still many unanswered questions regarding the micromechanics of the alveolus and how it deforms during lung inflation. Therefore, the aims of this review are to draw a multidisciplinary account of the mechanics of the alveolus on the basis of its structure, biology, and chemistry and to compare estimates of alveolar deformation from previous studies.

Static and dynamic imaging of alveoli using optical coherence tomography needle probes

“…For instance, the mechanisms of lung volume expansion have been widely discussed in the literature (14,47), yet no established unifying model of alveolar mechanics has been accepted. A key question is whether alveoli are recruited during respiration or whether they follow some model of expansion.…”

Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction

“…Plasma membrane unfolding and deformation-induced lipid trafficking along with cytoskeletal remodeling prevent cell wounding. However, in injured, mechanically ventilated lungs, the forces acting on the cells might be excessive or abrupt, increasing the risk of failure of these cell load-bearing components (175,197). Excessive opening and closing of alveoli, termed cyclic stretch (CS), induces lung damage by directly wounding alveolar epithelial cells and also by affecting epithelial cell-cell interactions (46, 175).…”

Coming to terms with tissue engineering and regenerative medicine in the lung

“…For example, even brief periods of alveolar stretch can induce an inflammatory cascade (227) that can in turn influence alveoli and the pulmonary vasculature. Here, the extent of stretch is likely important (8,40,163,195), and stretch effects may involve a range of pathways including Fas/FasL (93), Rac1 (41), PLA2 (116), GEF-H1 (17), caveolins (222), and Rho kinase (42), with modulating effects of oxygen (78,164), ROS (31), and inflammation per se (72,82).…”