Immunohistochemical study for the expression of leukocyte adhesion molecules, and FGF23 and ACE2 in P. gingivalis LPS-induced diabetic nephropathy.
Immunohistochemical study for the expression of leukocyte adhesion molecules, and FGF23 and ACE2 in P. gingivalis LPS-induced diabetic nephropathy.
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DOI：
10.1186/s12882-020-02203-y
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发表时间：
2021-01-06
期刊：
影响因子：
2.3
通讯作者：
Tamaoki S
中科院分区：
文献类型：
--
作者：
Kajiwara K;Sawa Y;Fujita T;Tamaoki S
本研究旨在探讨白细胞粘附分子和肾脏代谢因子在糖尿病小鼠牙周病原体pg - lps肾病中的表达。我们最近报道了糖尿病环境下肾小球内皮表达toll样受体（TLR）2和TLR4， TLR2/4配体牙龈卟啉单胞菌脂多糖（Pg-LPS）诱导糖尿病小鼠肾病。认为Pg-LPS通过TLR对糖尿病肾脏的识别，通过白细胞粘附分子和肾脏特异性代谢酶的过度表达促进慢性炎症。目前还没有关于牙周病细菌对肾内白细胞粘附分子表达和生理活性物质积累影响的报道。采用免疫组化方法对糖尿病小鼠肾脏pg - lps诱导肾病伴肾小球硬化进行研究。链脲佐剂（STZ）诱导的糖尿病ICR小鼠（STZ-ICR）和健康ICR小鼠（Pg-LPS -ICR）均无血管表达血管细胞粘附分子-1 （VCAM-1）、e-选择素或成纤维细胞生长因子（FGF） 23。然而，在糖尿病ICR小鼠肾伴pg - lps诱导的肾病（LPS-STZ）中，在肾小管和肾小球中观察到VCAM-1的表达和FGF23的积累，在肾实质和肾小球中观察到e -选择素的表达。血管紧张素转换酶2 （ACE2）在近端小管中检测到，但在ICR、STZ-ICR或LPS-ICR的其他区域未检测到。LPS-STZ在肾小管和肾小球中均检测到ACE2。糖尿病患者肾实质中Mac-1和podoplanin阳性细胞增多，LPS-STZ中有大量Mac-1阳性细胞分布。Pg-LPS可通过肾小球内VCAM-1和e -选择素的过表达，诱导Mac-1/podoplanin阳性巨噬细胞浸润，引起肾小球硬化和小管炎等糖尿病性肾脏炎症，导致ACE2和FGF23的积累，而这两种物质在糖尿病条件下的炎症性肾损伤中未代谢。牙周炎可能是糖尿病肾病进展的关键因素。
The present study aims to examine the expression of leukocyte adhesion molecules and renal metabolic factors in diabetic mouse kidneys with periodontal pathogen Pg-LPS-induced nephropathy. We recently reported that the glomerular endothelium expresses toll-like receptor (TLR)2 and TLR4 in diabetic environments and TLR2/4 ligand Porphyromonas (P.) gingivalis lipopolysaccharides (Pg-LPS) induce nephropathy in diabetic mice. It is thought that Pg-LPS promotes the chronic inflammation with the overexpression of leukocyte adhesion molecules and renal-specific metabolic enzymes by the recognition of Pg-LPS via TLR in the diabetic kidneys. There have been no reports of the effects of periodontopathic bacteria on the expression of leukocyte adhesion molecules and the accumulation of physiologically active substances in the kidney. The immunohistochemical investigation was performed on diabetic mouse kidney with Pg-LPS-induced nephropathy with glomerulosclerosis in glomeruli. There were no vessels which expressed vascular cell adhesion molecule-1 (VCAM-1), E-selectin, or fibroblast growth factor (FGF) 23 in streptozotocin (STZ)-induced diabetic ICR mice (STZ-ICR), or in healthy ICR mice administered Pg-LPS (LPS-ICR). However, in diabetic ICR mouse kidneys with Pg-LPS-induced nephropathy (LPS-STZ) the expression of VCAM-1 and the accumulation of FGF23 were observed in renal tubules and glomeruli, and the expression of E-selectin was observed in renal parenchyma and glomeruli. The angiotensin-converting enzyme 2 (ACE2) was detected in the proximal tubules but not in other regions of ICR, STZ-ICR, or LPS-ICR. In LPS-STZ ACE2 was detected both in renal tubules as well as in glomeruli. The Mac-1 and podoplanin-positive cells increased in the renal parenchyma with diabetic condition and there was the distribution of a large number of Mac-1-positive cells in LPS-STZ. The Pg-LPS may induce diabetic renal inflammation such as glomerulosclerosis and tubulitis with infiltration of Mac-1/podoplanin positive macrophages via glomerular overexpression of VCAM-1 and E-selectin, resulting in accumulation of both ACE2 and FGF23 which were unmetabolized with the inflammation-induced kidney damage under the diabetic condition. Periodontitis may be a critical factor in the progress of nephropathy in diabetic patients.
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影响因子：
4.2
作者：
Li, Fanglin;Yang, Niansheng;Yu, Xueqing
通讯作者：
Yu, Xueqing
影响因子：
18.6
作者：
Garcia, RI;Henshaw, MM;Krall, EA
通讯作者：
Krall, EA
DOI：
10.1152/ajprenal.00319.2012
发表时间：
2012-10-01
影响因子：
4.2
作者：
Kaur, Harmeet;Chien, Alexander;Jialal, Ishwarlal
通讯作者：
Jialal, Ishwarlal
影响因子：
6.1
作者：
Hauser, IA;Riess, R;Sterzel, RB
通讯作者：
Sterzel, RB
牙龈卟啉单胞菌脂多糖通过 Toll 样受体促进肾病。
影响因子：
4.8
作者：
Kajiwara K;Takata S;To TT;Takara K;Hatakeyama Y;Tamaoki S;Darveau RP;Ishikawa H;Sawa Y
通讯作者：
Sawa Y