An immunohistochemical study on the expression of bioactive molecules in the mouse kidney in P. gingivalis LPS-induced diabetic nephropathy

Abstract: Diabetic nephropathy is a serious complication of diabetes mellitus, which is caused by glomerulosclerosis with renal failure based on the dysfunction of glomerular capillaries. We recently reported that the glomerular endothelium in the glomeruli of diabetic mice expresses toll-like receptor (TLR)2 and TLR4, and that Porphyromonas (P.) gingivalis lipopolysaccharide (LPS) induces diabetic nephropathy with urinary protein and the accumulation of type 1 collagen, IL-6, TNF-α, and TGF-β in glomeruli. This study aims to immunohistochemically investigate the expression of leukocyte adhesion molecules, and renal physiologically active molecule FGF23 and SARS-CoV-2 receptor ACE2 in the glomeruli of P. gingivalis LPS induced-diabetic nephropathy model mouse. All of the diabetic mice subjected to repeated P. gingivalis LPS administrations were euthanized within the survival period of all diabetic mice not administered LPS and within the survival period of all of the LPS-administered non-diabetic mice. The VCAM-1, E-selectin, FGF23, and ACE2 were overexpressed in the glomeruli of P. gingivalis LPS induced-diabetic nephropathy in mice although these molecules were not found in LPS-administered normal kidney and non LPS-administered diabetic mice. It is thought that the P. gingivalis is one of the critical factors in the diabetic patients.