Abstract
Introduction: The lung surfactant dipalmitoylphosphatidylcholine (DPPC) leaks into the blood, settling on the luminal aspect of blood vessels to create active hydrophobic spots. Nanobubbles are formed at these spots from dissolved gas. We hypothesized that when a large molecule in the blood comes into contact with a nanobubble at the active hydrophobic spots, its tertiary structure is disrupted. An exposed epitope may then prompt an autoimmune response. In a previous study, plasma DPPC in diabetes type 1 was higher in 2 samples from patients within 1.5 years in the disease compared to 8 others from longer time in the disease. Could these 1.5 years represent the previous time when active hydrophobic spots were formed?
Methods: DPPC was measured in plasma of 10 diabetes type 1 patients within 1.5 years in the disease compared to 10 controls.
Results: DPPC in the diabetic group was 1.17 ± 0.27 µg/ml , non-significantly higher than in the control group (1.51 ± 0.42 µg/ml ).
Discussion: Leakage of DPPC from the lung to the plasma is not the limiting factor for buildup of the active hydrophobic spots. The heart of lupus mice contained more DPPC from the control mice. Further investigation, should explore the content of DPPC in the blood vessels from diabetic animals. If our hypothesis is proved true, it may open up considerable therapeutic potential.