Pulmonary surfactant

Also known as: surfactant, DPPC, lecithin, surfactant proteins

A lipoprotein film secreted by type II pneumocytes that lowers alveolar surface tension, stabilising alveoli, increasing compliance and keeping the alveoli dry.

Overview

Composition≈90% lipid (DPPC chief), ≈10% protein (SP-A, B, C, D)

Surface tension at FRC≈25 mN/m (vs ≈70 mN/m for water)

Surfactant is ≈90% lipid — mainly phospholipids, of which dipalmitoylphosphatidylcholine (DPPC) is the principal surface-active component, plus phosphatidylglycerol and cholesterol — and ≈10% protein. The hydrophobic SP-B and SP-C are essential for rapid adsorption and spreading of the film; the hydrophilic collectins SP-A and SP-D bind and opsonise microbes and modulate inflammation.

At the air–liquid interface the DPPC molecules orient with hydrophobic tails towards air, opposing the attractive forces between water molecules. Surface tension falls from ≈70 mN/m (water) to ≈25 mN/m at FRC and close to zero as the film is compressed during expiration. Because the film is compressed more in smaller alveoli, it lowers their surface tension more, counteracting the Laplace relationship (P = 2T/r) and preventing small alveoli from emptying into large ones. Lower surface tension also reduces the work of breathing, increases compliance, explains hysteresis of the pressure–volume curve, and decreases the suction of fluid from capillaries into alveoli.

Location

As a thin film lining the alveolar surface (and to a lesser extent the small airways).

Function

Lowers surface tension, increasing lung compliance and reducing the work of breathing.

Stabilises alveoli of different sizes (prevents atelectasis).

Keeps alveoli dry by reducing transudation of fluid.

Innate immune defence (SP-A, SP-D).

Secretions

Secreted by exocytosis of lamellar bodies from type II pneumocytes; recycled by type II cells and degraded by alveolar macrophages.

Regulation

Production increases late in gestation (adequate by ≈34–35 weeks) and is stimulated by glucocorticoids, thyroid hormones, β-agonists and periodic deep breaths (sighs); fetal hyperinsulinaemia (maternal diabetes) delays it.

Clinical significance

Neonatal respiratory distress syndrome

Surfactant deficiency in preterm infants: stiff lungs, progressive atelectasis and hyaline membranes. Prevention with antenatal corticosteroids; treatment with exogenous (animal-derived) surfactant via the endotracheal tube plus CPAP.

Acquired surfactant dysfunction

In ARDS, plasma proteins leaking into alveoli inactivate surfactant; after cardiopulmonary bypass and with prolonged high-O2 breathing, surfactant production falls, promoting atelectasis.

Test yourself

According to the law of Laplace, why would small alveoli collapse into larger ones in the absence of surfactant?

Small alveoli have a lower surface tension
The collapsing pressure is inversely proportional to alveolar radius
Large alveoli have a higher collapsing pressure
Surface tension is proportional to alveolar volume

Answer: The collapsing pressure is inversely proportional to alveolar radius

P = 2T/r. At equal surface tension, a smaller radius generates a greater collapsing pressure, so a small alveolus would empty into a larger one. Surfactant lowers T more in small alveoli (where its molecules are compressed together), equalising pressures and stabilising alveoli.

Which cell secretes pulmonary surfactant?

Type II pneumocyte
Type I pneumocyte
Club (Clara) cell only
Alveolar macrophage

Answer: Type II pneumocyte

Cuboidal type II pneumocytes store surfactant (mainly dipalmitoylphosphatidylcholine plus surfactant proteins A–D) in lamellar bodies and secrete it by exocytosis. They are also progenitors that replace type I cells after injury. Club cells secrete some surfactant-like proteins in bronchioles but are not the main source.