Pulmonary surfactant

Pulmonary surfactant is a surface-active complex of phospholipids and proteins formed by type II alveolar cells.

By adsorbing to the air-water interface of alveoli, with hydrophilic head groups in the water and the hydrophobic tails facing towards the air, the main lipid component of the surfactant, dipalmitoylphosphatidylcholine (DPPC), reduces surface tension.

The components for these lipids diffuse from the blood into type II alveolar cells where they are assembled and packaged for secretion into secretory organelles called lamellar bodies.

The SP proteins reduce the critical temperature of DPPC's phase transition to a value lower than 37 °C,[10] which improves its adsorption and interface spreading velocity.

Each SP protein has distinct functions, which act synergistically to keep an interface rich in DPPC during lung's expansion and contraction.

Ex-situ measurements of surface tension and interfacial rheology can help to understand the functionality of pulmonary surfactants.

Because during ventilation there is a variation of the lung surface area, the surfactant's interface concentration is not usually at the level of saturation.

Thus, the surfactant density at the air water interface remains high and is relatively preserved throughout expiration, decreasing the surface tension even further.

[citation needed] SP molecules contribute to increasing the surfactant interface adsorption kinetics, when the concentration is below the saturation level.

[11][13][14] Surfactant production in humans begins in type II cells during the alveolar sac stage of lung development.

[16] These lamellar bodies are secreted by exocytosis into the alveolar lining fluid, where the surfactant forms a meshwork of tubular myelin[17][18] Full term infants are estimated to have an alveolar storage pool of approximately 100 mg/kg of surfactant, while preterm infants have an estimated 4–5 mg/kg at birth.

Up to 90% of surfactant DPPC (dipalmitoylphosphatidylcholine) is recycled from the alveolar space back into the type II pneumocyte.

In late 1920s von Neergaard[22] identified the function of the pulmonary surfactant in increasing the compliance of the lungs by reducing surface tension.

Later, in the middle of the 1950s, Pattle and Clements rediscovered the importance of surfactant and low surface tension in the lungs.

At the end of that decade it was discovered that the lack of surfactant caused infant respiratory distress syndrome (IRDS).