Abstract
Introduction The lung surfactant dipalmitoylphosphatidylcholine 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 contact between a large molecule in the blood at the gaseous/liquid interface would disrupt the molecule’s tertiary structure. An exposed epitope may then prompt an autoimmune response. The double cause hypothesis suggests that high level of DPPC is a prerequisite for the development of autoimmune disease. The double cause hypothesis was supported in a study using diabetic mice.
Methods dipalmitoylphosphatidylcholine content was determined in the hearts of mice which suffered lupus: those which contracted lupus (lpr) and their control which would contract the disease much later on (mjp) and healthy control mice strain (C57/BL6).
Results dipalmitoylphosphatidylcholine content (mg/g, mean ± SD) in the three groups was: for lpr 32.1 ± 4.7, for mjp 36.1 ± 7.7 and for the control C57/BL6 40.3 ± 10.4. There was no significant difference between the three groups.
Discussion We suggest that the difference between diabetic mice and lupus is due to the nature of autoantigens: a protein in diabetic and nuclear, ribonucleoproteins and ribosomes in lupus. Possibly the distortion at the gaseous/liquid interface is more pronounced in proteins.