The lung surfactant dipalmitoylphosphatidylcholine (DPPC) most probably leaks into the blood, settling on the luminal aspect of blood vessels to create active hydrophobic spots (AHS). 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 AHS, its tertiary structure is disrupted. An epitope not previously having undergone thymus education may then prompt an autoimmune response. There are thus two independent processes which may share the blame for autoimmune disease: spillage of large molecules into the blood, and the creation of AHS. DPPC was measured in 10 diabetes type 1 patients and 10 control subjects. DPPC in the diabetic group was 4.63 ± 0.68 μg/mL, non-significantly higher than in the control group (4.23 ± 0.94 μg/mL). However, in the diabetic group, DPPC was high when the samples were taken within 1.5 years of disease onset. This is closer to the time of AHS production, which takes place ahead of the disease. Further investigation, with sampling for DPPC as soon as possible after onset of the disease, may provide additional support for our hypothesis. If proved true, this may open up considerable therapeutic potential.

肺表面活性剂二棕榈酰磷脂酰胆碱 (DPPC) 很可能会渗入血液中，在血管腔内形成活性疏水点 (AHS)。纳米气泡在这些点由溶解的气体形成。我们假设，当血液中的一个大分子与 AHS 处的纳米气泡接触时，其三级结构就会被破坏。之前没有接受过胸腺教育的表位可能会引发自身免疫反应。因此，有两个独立的过程可能会导致自身免疫性疾病：大分子溢出到血液中，以及 AHS 的产生。在 10 名 1 型糖尿病患者和 10 名对照受试者中测量了 DPPC。糖尿病组的 DPPC 为 4.63 ± 0.68 μg/mL，不显着高于对照组（4.23 ± 0.94 μg/mL）。然而，在糖尿病组中，在疾病发病 1.5 年内采集样本时，DPPC 较高。这更接近于 AHS 生产的时间，它发生在疾病之前。进一步调查，在疾病发作后尽快对 DPPC 进行采样，可能为我们的假设提供额外的支持。如果证明属实，这可能会带来相当大的治疗潜力。