Pulmonary Surfactant: A Mighty Thin Film

Abstract

Pulmonary surfactant is a critical component of lung function in healthy individuals. It functions in part by lowering surface tension in the alveoli, thereby allowing for breathing with minimal effort. The prevailing thinking is that low surface tension is attained by a compression-driven squeeze-out of unsaturated phospholipids during exhalation, forming a film enriched in saturated phospholipids that achieves surface tensions close to zero. A thorough review of past and recent literature suggests that the compression-driven squeeze-out mechanism may be erroneous. Here, we posit that a surfactant film enriched in saturated lipids is formed shortly after birth by an adsorptiondriven sorting process and that its composition does not change during normal breathing. We provide biophysical evidence for the rapid formation of an enriched film at high surfactant concentrations, facilitated by adsorption structures containing hydrophobic surfactant proteins. We examine biophysical evidence for and against the compressiondriven squeeze-out mechanism and propose a new model for surfactant function. The proposed model is tested against existing physiological and pathophysiological evidence in neonatal and adult lungs, leading to ideas for biophysical research, that should be addressed to establish the physiological relevance of this new perspective on the function of the mighty thin film that surfactant provides.

Microplastics and Nanoplastics Impair the Biophysical Function of Pulmonary Surfactant by Forming Heteroaggregates at the Alveolar–Capillary Interface

“…It was found that the addition of MPs/NPs significantly decreases the vesicle size of Infasurf (Figure S4). This indicates denaturation of surfactant-associated proteins (SP-B/C), since these small, hydrophobic proteins promote the formation of large vesicular aggregates by inducing membrane fusion. , Decreasing phospholipid vesicle size in natural pulmonary surfactants is a strong indication of surfactant inhibition. , Figure depicts the main findings and the EHS impact of this study.…”

The Underlying Mechanism of Poisoning after the Accidental Inhalation of Aerosolised Waterproofing Spray

“…We have previously suggested that the biological target of poisonings by the inhalation of waterproofing products is the lung surfactant in the respiratory parts of the lungs [11]. Lung surfactant is secreted into the thin liquid lining covering the respiratory parts of the lungs, where it regulates surface tension at the air-liquid interface in the alveoli [12,13]. The regulation of surface tension during breathing is essential for normal lung function, and the disruption of lung surfactant function can lead to decreased lung function, as described in an adverse outcome pathway [14] and https://aopwiki.org/aops/302 (accessed on 1 March 2024).…”

Structure and Function of Canine SP-C Mimic Proteins in Synthetic Surfactant Lipid Dispersions

“…Lung surfactant is a mixture of lipids and proteins synthesized by alveolar type 2 cells and secreted into the lung alveoli where it reduces surface tension at the air-liquid interface [1,2]. Mammalian lung surfactant contains about 80% phospholipids, 10% neutral lipids, and 10% protein.…”