Surfactant Proteins-A and -B Are Elevated in Plasma of Patients with Acute Respiratory Failure

Abstract

Surfactant protein-A (SP-A) leaks into the circulation of patients with acute respiratory distress syndrome (ARDS) or acute cardiogenic pulmonary edema (APE) in a manner inversely related to lung function. Since surfactant protein-B (SP-B) is synthesized as a precursor considerably smaller than alveolar SP-A, we investigated whether it enters the circulation more readily. Reactivities consistent with SP-B proprotein (approximately 42 to approximately 45 kD) and the approximately 25 kD processing intermediate were detected in plasma. Plasma immunoreactive SP-B levels were significantly higher in ARDS (8,007+/-1,654 ng/ml [mean+/-SEM], n = 22) and APE (3,646+/-635 ng/ml, n = 10) patients compared with normal subjects (1,685+/-58 ng/ml, n = 33) and ventilated patients with no cardiorespiratory disease (1,829+/-184 ng/ml, n = 7). All groups had plasma SP-B/SP-A ratios approximately 6- to approximately 8-fold higher than in normal lavage or ARDS tracheal aspirate fluid, consistent with protein sieving. During admission, both plasma SP-B and the SP-B/SP-A ratio were inversely related to blood oxygenation (PaO2/FIO2) (p < 0.0001 and p < 0.025, n = 260 from 39 patients; Spearman) and static respiratory system compliance (deltaV/deltaP) (p < 0.0001 and p < 0.01, n = 168 from 25 patients). We describe in detail three patients and conclude that immunoreactive SP-B enters more readily than SP-A, is cleared acutely, and provides a better indicator of lung trauma.

Study of Role of Surfactant Protein-D, Malondialdehyde, Protein Carbonyl and its Correlation with Airflow Obstruction (FEV1% Predicted) in Patients with Smoker Chronic Obstructive Pulmonary Disease (COPD)

“…In our study we found increase levels of SP-D in patients with smoker COPD and non-smoker COPD this might be due to deleterious effects oxidants from tobacco smoke and oxidants originated from endogenous sources on lung tissue cause release of SP-D in blood stream. The increased level of SP-D in the blood stream depends on the extent of injury to the lung tissue and is directly related to pulmonary function [25][26][27]. In our study we obtain inverse correlation between SP-D with FEV1% predicted and FEV1/FVC % ratio in COPD patients.…”

Chemokines Accumulate in the Lungs of Rats with Severe Pulmonary Embolism Induced by Polystyrene Microspheres

“…Many of these proteins were also abundant in plasma and were presumably plasma-derived, as has been previously suggested (51,52). The flow of proteins across the alveolar-capillary wall is bidirectional in normal lungs: plasma proteins enter the alveoli down a steep pressure gradient, while lung-specific surfactant proteins, present in high concentrations on the alveolar epithelial lining surface, normally diffuse across the capillary wall down their own steep concentration gradients and can be detected in blood (53,54). Under conditions of pulmonary artery hypertension, the in-flow of plasma proteins across the capillary wall would likely be increased while the rate of absorption of surfactant into the blood or lymph would be reduced.…”

Pneumoproteinaemia: a new perspective in the assessment of lung disorders

“…Another pneumoprotein is surfactant-associated protein A (SP-A), a ~28-35 kDa protein mainly secreted by alveolar type II cells, occurring in the respiratory tract and serum in monomeric and various oligomeric forms [14,15]. Similar findings have been made with the ~18 kDa surfactantassociated protein B (SP-B), secreted by both alveolar and bronchiolar cells [16].…”