4.4 Review

The micromechanics of lung alveoli: structure and function of surfactant and tissue components

Journal

HISTOCHEMISTRY AND CELL BIOLOGY
Volume 150, Issue 6, Pages 661-676

Publisher

SPRINGER
DOI: 10.1007/s00418-018-1747-9

Keywords

Acinus; Type II alveolar epithelial cell; Surfactant; Connective tissue; Acute lung injury; Fibrosis

Funding

  1. German Research Federation (DFG) [OC23/7-3, OC23/8-1, OC23/9-3, OC23/10-1, KN916/1-1, SFB 587/TP B18, INST 192/504-1, INST 193/57-1]
  2. Federal Ministry for Education and Research (BMBF: German Center for Lung Research DZL) [01DG14009]
  3. Swiss National Science Foundation (SNF) [116417, 121390, CRSII3_ 160704/1]
  4. Swiss National Science Foundation (SNF) [CRSII3_160704] Funding Source: Swiss National Science Foundation (SNF)

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The mammalian lung ' s structural design is optimized to serve its main function: gas exchange. It takes place in the alveolar region (parenchyma) where air and blood are brought in close proximity over a large surface. Air reaches the alveolar lumen via a conducting airway tree. Blood flows in a capillary network embedded in inter-alveolar septa. The barrier between air and blood consists of a continuous alveolar epithelium (a mosaic of type I and type II alveolar epithelial cells), a continuous capillary endothelium and the connective tissue layer in-between. By virtue of its respiratory movements, the lung has to withstand mechanical challenges throughout life. Alveoli must be protected from over-distension as well as from collapse by inherent stabilizing factors. The mechanical stability of the parenchyma is ensured by two components: a connective tissue fiber network and the surfactant system. The connective tissue fibers form a continuous tensegrity (tension+integrity) backbone consisting of axial, peripheral and septal fibers. Surfactant (surface active agent) is the secretory product of type II alveolar epithelial cells and covers the alveolar epithelium as a biophysically active thin and continuous film. Here, we briefly review the structural components relevant for gas exchange. Then we describe our current understanding of how these components function under normal conditions and how lung injury results in dysfunction of alveolar micromechanics finally leading to lung fibrosis.

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