Abstract

Ravasio A, Hobi N, Bertocchi C, Jesacher A, Dietl P, Haller T. Interfacial sensing by alveolar type II cells: a new concept in lung physiology? Am J Physiol Cell Physiol 300: C1456-C1465, 2011. First published January 26, 2011; doi: 10.1152/ajpcell.00427.2010.-Alveolar type II (AT II) cells are in close contact with an air-liquid interface (I-AL). This contact may be of considerable physiological relevance; however, no data exist to provide a satisfying description of this specific microenvironment. This is mainly due to the experimental difficulty to manipulate and analyze cell-air contacts in a specific way. Therefore, we designed assays to quantify cell viability, Ca2+ changes, and exocytosis in the course of interface contact and miniaturized I-AL devices for direct, subcellular, and real-time analyses of cell-interface interactions by fluorescence microscopy or interferometry. The studies demonstrated that the sole presence of an I-AL is not sensed by the cells. However, when AT II cells are forced into closer contact with it, they respond promptly with sustained Ca2+ signals and surfactant exocytosis before the occurrence of irreversible cell damage. This points to a paradoxical situation: a potential threat and potent stimulus for the cells. Furthermore, we found that the signalling mechanism underlying sensation of an I-AL can be sufficiently explained by mechanical forces. These results demonstrate that the I-AL itself can play a major, although so-far neglected, role in lung physiology, particularly in the regulatory mechanisms related with surfactant homeostasis. Moreover, they also support a general new concept of mechanosensation in the lung.