Int J Med Sci 2021; 18(12):2661-2665. doi:10.7150/ijms.55648

Short Research Paper

β3-integrin Leu33Pro gain of function variant does not modulate inflammatory activity in human derived macrophages in diabetes

Philipp Helmer1✉, Ellen Damm1, Stephan Schiekofer2,3, Kirsten Roomp4, Jochen G. Schneider1,4✉

1. Saarland University, Medical Center, Dpt. of Internal Medicine II, Homburg, Saar, Germany.
2. Zentrum für Altersmedizin, Klinik und Poliklinik für Psychiatrie und Psychotherapie der Universität Regensburg am Bezirksklinikum, Regensburg, Germany.
3. Sigmund Freud Privat-Universität, Wien, Austria.
4. Luxembourg Centre for Systems Biomedicine (LCSB), University of Luxembourg, Belvaux, Luxembourg, and Centre Hospitalier Emile Mayrisch, Esch/Alzette, Luxembourg.

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Citation:
Helmer P, Damm E, Schiekofer S, Roomp K, Schneider JG. β3-integrin Leu33Pro gain of function variant does not modulate inflammatory activity in human derived macrophages in diabetes. Int J Med Sci 2021; 18(12):2661-2665. doi:10.7150/ijms.55648. Available from https://www.medsci.org/v18p2661.htm

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Abstract

Objective: We aimed to investigate the association between the Leu33Pro (rs5918) polymorphism in β3-integrin with diabetic complications and inflammatory function of macrophages depending on the genotype in subjects with diabetes mellitus.

Material and methods: We determined the Leu33Pro polymorphism in 186 diabetic subjects and collected laboratory data. Monocytes from 24 patients were collected for macrophage differentiation to determine the inflammatory activity by treating with different stimulants.

Results: We could demonstrate that human derived differentiated macrophages expressed β3‑integrin. Their secretory capacity upon inflammatory stimulation did not reveal any differences depending on the Leu33Pro variant. We found trends for an association of the polymorphism with the presence of diabetic nephropathy (p = 0.071), as well as with creatinine [1.32 mg/dL (1) vs. 0.98 mg/dL (0)] (p = 0.029 in recessive model) and glomerular filtration rate [75.6 ml/min ± 22 vs. 62.3 ml/min ± 25] (p = 0.076 in recessive model) as quantitative markers of kidney function.

Conclusion: Despite the expression of β3‑integrin in human macrophages, the Leu33Pro polymorphism in β3‑integrin does not modify the inflammatory response upon stimulation but might play a role in the progression of diabetic nephropathy. Further studies are necessary to substantiate such a hypothesis.

Keywords: Leu33Pro polymorphism, rs5918, diabetes, diabetic nephropathy, inflammation, macrophages