Role of Lung Surfactant in Respiratory Disease: Current Knowledge in Large Animal Medicine

Abstract

Lung surfactant is produced by type II alveolar cells as a mixture of phospholipids, surfactant proteins, and neutral lipids. Surfactant lowers alveolar surface tension and is crucial for the prevention of alveolar collapse. In addition, surfactant contributes to smaller airway patency and improves mucociliary clearance. Surfactant-specific proteins are part of the innate immune defense mechanisms of the lung. Lung surfactant alterations have been described in a number of respiratory diseases. Surfactant deficiency (quantitative deficit of surfactant) in premature animals causes neonatal respiratory distress syndrome. Surfactant dysfunction (qualitative changes in surfactant) has been implicated in the pathophysiology of acute respiratory distress syndrome and asthma. Analysis of surfactant from amniotic fluid allows assessment of fetal lung maturity (FLM) in the human fetus and exogenous surfactant replacement therapy is part of the standard care in premature human infants. In contrast to human medicine, use and success of FLM testing or surfactant replacement therapy remain limited in veterinary medicine. Lung surfactant has been studied in large animal models of human disease. However, only a few reports exist on lung surfactant alterations in naturally occurring respiratory disease in large animals. This article gives a general review on the role of lung surfactant in respiratory disease followed by an overview of our current knowledge on surfactant in large animal veterinary medicine.

Serum Levels of Surfactant Proteins in Patients with Combined Pulmonary Fibrosis and Emphysema (CPFE)

“…Second, patients were followed up for only one year which is probably the reason for the lack for any significant associations regarding SPs and survival in patients with emphysema and CPFE. Finally, it is a fact that SP-A and SP-D are additionally produced in several extrapulmonary locations, including the brain, the salivary glands, the heart, the kidneys and the reproductive tract [ 71 ] and for this reason we cannot confirm that the levels that are measured in serum directly originate from the lung. However, since the greater amounts of all four surfactant proteins are synthesized by alveolar type II cells and SP-A, SP-B and SP-D are also produced by different types of airway cells, including Clara cells and submucosal cells, we can conclude that the major source of serum SP levels comes from the pulmonary epithelium.…”

Cardiac biomarkers in premature calves with respiratory distress syndrome

“…In this study, premature calves had clinical signs related to RDS, including low venous pH, pO 2 and O 2 saturation and high pCO 2 consistent with dyspnoea, hypoxaemia, and inadequate oxygen delivery (Table 2). High alveolar surface tension due to the lack of surfactant is likely to result in extensive alveo-lar collapse leading to pulmonary atelectasia, ventilation-perfusion incompatibility, hypoxaemia, hypercapnia, and respiratory acidosis (Christmann et al, 2009).…”

Phosphatidylglycerol and surfactant: A potential treatment for COVID-19?

“…However, the initial presentation might be expected to show differences from the respiratory distress seen in pre-term infants: phosphatidylcholine represents approximately two-thirds to three-quarters of pulmonary surfactant lipid content [45] , [46] and thus provides the majority of its surfactant activity. Therefore, gradual loss of phosphatidylcholine would allow maintenance of compliance despite enhanced inflammation resulting from decreased levels of PG, which comprises only 9–12% of surfactant phospholipid [45] , [46] , and the resultant pulmonary edema. Presumably, loss of the anti-surface tension effects of surfactant would only occur once large numbers of Type II alveolar cells were destroyed and phosphatidylcholine was severely depleted.…”