ABSTRACT
Although surfactant-related functions of type II cells are emphasized here, these cells have multiple roles in pulmonary biology and pathobiology ([212, 218, 258, 698, 1195] for review). Alveolar type II epithelial cells respond to and produce multiple cytokines, growth factors, and other mediators and products during lung growth, development, inflammation, injury, and repair. Examples of the many mediators produced by type II cells include transforming growth factors (TGF) α and β; interleukin (IL)-6, 8, 11; tumor necrosis factor (TNF) α; various complement components; monocyte chemoattractant protein (MCP)-1; and granulocyte-macrophage colony stimulating factor (GM-CSF) . Type II cells also respond to these mediators plus a host of other self-produced or externally elaborated factors including keratinocyte growth factor (KGF), epidermal growth factor (EGF), hepatocyte growth factor (HGF), fibroblast growth factor (FGF), IL-1, and many more. Some of the specific mediators that affect and help regulate surfactant metabolism in type II cells are noted in the following section. In addition to lung surfactant, type II cells produce a variety of products including
Figure 6-8 Alveolar type II epithelial cell. A type II cell from adult human lung shows characteristic cytoplasmic lamellar body organelles under electron microscopy. These organelles contain stored pulmonary surfactant. Type II pnuemocytes are the primary cells of lung surfactant metabolism. They are also stem cells for the alveolar epithelium and play other roles in pulmonary biology. Magnification ×8,000. (From Ref. 698 with permission.)
extracellular matrix components like fibronectin, collagen, proteoglycans, and many others. Type II cells and their products and responses affect not only the alveolar epithelium and extracellular matrix but also the pulmonary microvasculature, airways, and interstitium. The role of type II cells as stem cells for the alveolar epithelium is particularly important. In many forms of lung injury, type I cells are damaged, causing type II cells to proliferate and dedifferentiate to repopulate the epithelium (e.g., [96, 1194]). Type II cell alterations during lung injury, whether direct or indirect, can add a component of surfactant deficiency into the pathophysiology of acute lung injury (Chapter 10).
