TY - JOUR
T1 - Is the probable spillage of the lung surfactant dipalmitoylphosphatidylcholine the ultimate source of diabetes type 1?
AU - Arieli, Ran
AU - Khatib, Soliman
AU - Khattib, Aatef
AU - Bukovetzky, Elena
AU - Gottfried, Orna Dally
N1 - Publisher Copyright:
© 2021 Elsevier B.V.
PY - 2021/4
Y1 - 2021/4
N2 - 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.
AB - 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.
KW - Antigen
KW - Autoimmunity
KW - Coagulation
KW - DPPC
KW - Nanobubble
KW - Origin
UR - https://www.scopus.com/pages/publications/85099251396
U2 - 10.1016/j.resp.2020.103615
DO - 10.1016/j.resp.2020.103615
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C2 - 33421610
AN - SCOPUS:85099251396
SN - 1569-9048
VL - 286
JO - Respiratory Physiology and Neurobiology
JF - Respiratory Physiology and Neurobiology
M1 - 103615
ER -