The Double Cause Hypothesis for Autoimmune Diseases is Supported in Diabetic Mice (NOD)

Main Article Content

Nura Aburomi Soliman Khatib Ron Piran Ran Arieli

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 contact between a large molecule in the blood and a nanobubble at an active hydrophobic spot would disrupt the molecule’s tertiary structure. An exposed epitope may then prompt an autoimmune response.


Methods: DPPC content was determined in the heart of diabetic and healthy non-obese diabetic (NOD) mice and two control mice strains (C57/BL6 and Swiss-webster).


Results: The hearts from NOD mice contained more DPPC (47.6 ± 3.7 SE mg/g) than the control mice (36.9 ± 2.2 SE mg/g) (P < 0.018).


Discussion: It is probable that leakage of large β-cell molecules is the difference between affected and non-affected NOD mice. The Double Cause Hypothesis (DCH) is supported and the further research and applicability is discussed.

Keywords: lung surfactant, nanobubbles, heart, Active Hydrophobic Spot

Article Details

How to Cite
ABUROMI, Nura et al. The Double Cause Hypothesis for Autoimmune Diseases is Supported in Diabetic Mice (NOD). Medical Research Archives, [S.l.], v. 11, n. 12, dec. 2023. ISSN 2375-1924. Available at: <https://esmed.org/MRA/mra/article/view/4844>. Date accessed: 22 dec. 2024. doi: https://doi.org/10.18103/mra.v11i12.4844.
Section
Research Articles

References

1. Arieli R. Nanobubbles Form at Active Hydrophobic Spots on the Luminal Aspect of Blood Vessels: Consequences for Decompression Illness in Diving and Possible Implications for Autoimmune Disease-An Overview. Front Physiol. 2017;8:591. Published 2017 Aug 15. doi:10.3389/fphys.2017.00591
2. Arieli R. Was the appearance of surfactants in air breathing vertebrates ultimately the cause of decompression sickness and autoimmune disease?. Respir Physiol Neurobiol. 2015;206:15-18. doi:10.1016/j.resp.2014.11.008
3. Sutherland S. How auto-immunity starts. Sci. Am. 2021;325, September, 3: 39-36.
4. Eizirik DL, Colli ML, Ortis F. The role of inflammation in insulitis and beta-cell loss in type 1 diabetes. Nat Rev Endocrinol. 2009;5(4):219-226. doi:10.1038/nrendo.2009.21
5. Moyer MW. Women at risk. Sci. Am. 2021; 325, September, 3, 36-41
6. Arieli R, Khatib S. Dipalmitoylphosphatidylcholine in the heart of mice with lupus might support the hypothesis of dual causes of autoimmune diseases. Respir Physiol Neurobiol. 2022;300:103871. doi:10.1016/j.resp.2022.103871
7. Arieli R, Khatib S, Khattib A, Bukovetzky E, Gottfried OD. Is the probable spillage of the lung surfactant dipalmitoylphosphatidylcholine the ultimate source of diabetes type 1?. Respir Physiol Neurobiol. 2021;286:103615. doi:10.1016/j.resp.2020.103615
8. Arieli, R et al. Testing the Double Cause Hypothesis for Autoimmune Diseases, Dipalmitoylphosphatidylcholine Should be Measured in Plasma or Blood Vessels of Diabetes Type 1?. Medical Research Archives, [S.l.], v. 11, n. 4, apr. 2023.
9. Mallone R, Brezar V, Boitard C. T cell recognition of autoantigens in human type 1 diabetes: clinical perspectives. Clin Dev Immunol. 2011;2011:513210. doi:10.1155/2011/513210
10. Han S, Donelan W, Wang H, Reeves W, Yang LJ. Novel autoantigens in type 1 diabetes. Am J Transl Res. 2013;5(4):379-392. Published 2013 May 24.