Abstract
In 1977, Mason and Williams developed the concept of the alveolar epithelial type II (AE2) cell as a defender of the alveolus. It is well known that AE2 cells synthesise, secrete, and recycle all components of the surfactant that regulates alveolar surface tension in mammalian lungs. AE2 cells influence extracellular surfactant transformation by regulating, for example, pH and [Ca2+] of the hypophase. AE2 cells play various roles in alveolar fluid balance, coagulation/fibrinolysis, and host defence. AE2 cells proliferate, differentiate into AE1 cells, and remove apoptotic AE2 cells by phagocytosis, thus contributing to epithelial repair. AE2 cells may act as immunoregulatory cells. AE2 cells interact with resident and mobile cells, either directly by membrane contact or indirectly via cytokines/growth factors and their receptors, thus representing an integrative unit within the alveolus. Although most data support the concept, the controversy about the character of hyperplastic AE2 cells, reported to synthesise profibrotic factors, proscribes drawing a definite conclusion today.
Highlights
As early as 1954, CC Macklin had postulated some of the most important functions of the great pneumocyte, ie the pneumocyte type II or alveolar epithelial type II (AE2) cell (Fig. 1) [1]
By 1977, enough data had been collected to stimulate Mason and Williams [2] to formulate the concept of the AE2 cell as a “defender of the alveolus”
It was established that the main functions were synthesis and secretion of surface-active material, hyperplasia in reaction to alveolar epithelial injury, and serving as the progenitor for AE1 cells, which form the epithelial component of the thin air–blood barrier
Summary
As early as 1954, CC Macklin had postulated some of the most important functions of the great pneumocyte, ie the pneumocyte type II or alveolar epithelial type II (AE2) cell (Fig. 1) [1]. Transformation (conversion) Once released into the alveolar aqueous hypophase, the lamellar body material transforms into tubular myelin This is an amazingly regular phospholipid/SP-A assembly (Fig. 4), which gives rise to the surface-active lining layer from which, in turn, small vesicular forms derive that are thought to represent spent surfactant (for review, see [71]). Because intra-alveolar surfactant is highly susceptible to inactivation by serum proteins or reactive oxygen species (for review, see [176]), very few studies presented data indicating that the primary effect resulting in respiratory dysfunction was a defect in AE2 cells [177] It is still a matter of debate if hyperplastic AE2 cells, which are frequently observed in pathologic states (for reviews, see [144,178]) and which show altered expression patterns of many components and products [123], are beneficial or harmful to the alveolus. Most of the data collected to date support the concept of the AE2 cell as a defender of the alveolus, the controversy about the character of hyperplastic AE2 cells, proscribes drawing a definite conclusion
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