Effect of systemic administration of lipopolysaccharides derived from Porphyromonas gingivalis on gene expression in mice kidney

Harada, Fumiya; Uehara, Osamu; Morikawa, Tetsuro; Hiraki, Daichi; Onishi, Aya; Toraya, Seiko; Adhikari, Bhoj Raj; Takai, Rie; Yoshida, Koki; Sato, Jun; Nishimura, Michiko; Chiba, Itsuo; Wu, Chung Ze

doi:10.1007/s00795-018-0181-3

Cited by 12 publications

(19 citation statements)

References 27 publications

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“…In addition, upregulation of the expression levels of Saa3 , Ticam2 , Reg3b , Ocxt2a , and Xcr1 may be related to CKD pathogenesis. The five overexpressed genes in the kidney-derived endothelial cells were induced by LPS ( Harada et al, 2018 ). Each of these five genes has its own role.…”

Section: Impact Of Pd On the Pathogenesis Of Ckdmentioning

confidence: 99%

“…Reg3b regulates important biological processes such as immune responses, cell adhesion, and protection via apoptosis ( Ferreira et al, 2011 ). Increased Oxct2 expression may be related to diabetic CKD ( Harada et al, 2018 ). Both dendritic and endothelial cells may contribute to the overexpression of Xcr1 in the kidneys ( Lei and Takahama, 2012 ).…”

Section: Impact Of Pd On the Pathogenesis Of Ckdmentioning

confidence: 99%

“…Furthermore, periodontitis induced by periodontal pathogens can have an influence on and damage the kidneys. Harada et al (2018) studied the effect of gingival polysaccharide (PG-LPS) on the kidneys of mice. HE and PAS staining were performed on the kidneys for morphological and immunohistochemical analyses ( Harada et al, 2018 ).…”

Section: Association Between Pd and Ckdmentioning

confidence: 99%

“… Harada et al (2018) studied the effect of gingival polysaccharide (PG-LPS) on the kidneys of mice. HE and PAS staining were performed on the kidneys for morphological and immunohistochemical analyses ( Harada et al, 2018 ). The glomeruli were immunopositive for eNOS in the experimental group, but not in the control group.…”

Section: Association Between Pd and Ckdmentioning

confidence: 99%

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Periodontitis Exacerbates and Promotes the Progression of Chronic Kidney Disease Through Oral Flora, Cytokines, and Oxidative Stress

Zhang

Liu

et al. 2021

Front. Microbiol.

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Periodontitis is a type of systemic immune inflammation that is caused by the complex infection of a variety of microorganisms in the subgingival plaque and the imbalance of the microbial ecological environment in the mouth. Periodontitis and chronic kidney disease (CKD) share many risk factors, such as obesity, smoking, and age. A growing body of data supports a strong correlation between periodontitis and kidney disease. Evidence supports the role of periodontal inflammation and elevated serum inflammatory mediators in renal atherosclerosis, renal deterioration, and end-stage renal disease (ESRD) development. Periodontitis is a risk factor for kidney disease. However, to our knowledge, there are few studies detailing the possible link between periodontitis and CKD. This review summarizes the possible mechanisms underlying periodontitis and CKD. More importantly, it highlights novel and potential pathogenic factors for CKD, including bacteria, pro-inflammatory mediators and oxidative stress. However, most research on the relationship between periodontitis and systemic disease has not determined causality, and these diseases are largely linked by bidirectional associations. Future research will focus on exploring these links to contribute to new treatments for CKD.

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Section: Impact Of Pd On the Pathogenesis Of Ckdmentioning

confidence: 99%

Section: Impact Of Pd On the Pathogenesis Of Ckdmentioning

confidence: 99%

Section: Association Between Pd and Ckdmentioning

confidence: 99%

Section: Association Between Pd and Ckdmentioning

confidence: 99%

See 2 more Smart Citations

Periodontitis Exacerbates and Promotes the Progression of Chronic Kidney Disease Through Oral Flora, Cytokines, and Oxidative Stress

Zhang

Liu

et al. 2021

Front. Microbiol.

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“…Nevertheless, periodontal disease is a chronic inflammatory event and may not cause acute inflammatory changes in the pancreas. We previously developed a mouse model that is unaffected by acute inflammation with P. gingivalis lipopolysaccharide (PG-LPS) to observe the effect of LPS on the kidney [ 12 ]. The present study aimed to comprehensively explore the effects of systemic administration of PG-LPS on gene expression in the pancreas of these mice.…”

Section: Introductionmentioning

confidence: 99%

P. gingivalis Lipopolysaccharide Stimulates the Upregulated Expression of the Pancreatic Cancer-Related Genes Regenerating Islet-Derived 3 A/G in Mouse Pancreas

Hiraki

Uehara

Kuramitsu

et al. 2020

IJMS

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Although epidemiological studies have shown a relationship between periodontal disease and pancreatic cancer, the molecular mechanisms involved remain unclear. In this study, the effects of systemic administration of Porphyromonas gingivalis lipopolysaccharide (PG-LPS) on gene expression were comprehensively explored in mouse pancreas that did not demonstrate any signs of inflammation. PG-LPS was prepared in physiological saline and intraperitoneally administered to male mice at a concentration of 5 mg/kg every 3 days for 1 month. After extracting total RNA from the excised mice pancreas, a comprehensive DNA microarray analysis of gene expression was performed. Tissue specimens were also subjected to hematoxylin–eosin staining and immunohistochemistry using anti-regenerating islet-derived 3A and G (Reg3A/G) antibody. ImageJ software was used to quantify the area of Reg3A/G positive cells in pancreatic islets by binarizing image date followed by area extraction. The results were compared using Mann–Whitney U test. Data are presented as mean ± standard deviation (SD) with p < 0.05 considered as significant. Reg3G, a gene related to pancreatic cancer, was one of the 10 genes with the highest levels of expression in the pancreas stimulated with PG-LPS. The comprehensive analysis revealed a 73-fold increase in Reg3G expression level in the PG-LPS group when compared with the control group; in addition, the expression level of Reg3A was increased by 11-fold in the PG-LPS group. Image analysis showed that the ratio of Reg3A/G positive cells was higher in the PG-LPS group than the control. Immunostaining showed the presence of Reg3A/G-positive cells in the alpha-cell equivalent areas around the islets of Langerhans in the PG-LPS group. These results support the notion that periodontal disease may be a risk factor for pancreatic cancer.

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Melatonin improves periodontitis‐induced kidney damage by decreasing inflammatory stress and apoptosis in rats

Köse

Bayrakdar²,

Unver

et al. 2020

Journal of Periodontology

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Background Two main aims of this animal study were to inspect the possible effects of periodontitis on the structure and functions of the kidneys and the therapeutic effectiveness of melatonin. Methods Twenty‐four male Sprague‐Dawley rats were randomly divided into three groups: control, experimental periodontitis (Ep), and Ep‐melatonin (Ep‐Mel). Periodontitis was induced by placing 3.0‐silk sutures sub‐paramarginally around the cervix of right‐left mandibular first molars and maintaining the sutures for 5 weeks. Then melatonin (10 mg/kg body weight/day, 14 days), and the vehicle was administered intraperitonally. Mandibular and kidney tissue samples were obtained following the euthanasia. Periodontal bone loss was measured via histological and microcomputed tomographic slices. On right kidney histopathological and immunohistochemical, and on the left kidney biochemical (malonyl‐aldehyde [MDA], glutathione, oxidative stress [OSI], tumor necrosis factor [TNF]‐α, interleukin [IL]‐1β, matrix metalloproteinase [MMP]‐8, MMP‐9, and cathepsin D levels) evaluations were performed. Renal functional status was analyzed by levels of serum creatinine, urea, cystatin‐C, and urea creatinine. Results Melatonin significantly restricted ligature‐induced periodontal bone loss (P <0 .01) and suppressed the levels of proinflammatory cytokines (TNF‐α and IL‐1β), oxidative stress (MDA and OSI), and proteases (MMP‐8, MMP‐9, and CtD) that was significantly higher in the kidneys of the rats with periodontitis (P <0.05). In addition, periodontitis‐related histological damages and apoptotic activity were also significantly lower in the Ep‐Mel group (P <0.05). However, the markers of renal function of the Ep group were detected slightly impaired in comparison with the control group (P >0.05); and the therapeutic activity of melatonin was limited (P >0.05). Conclusion Melatonin restricts the periodontitis‐induced inflammatory stress, apoptosis, and structural but not functional impairments.

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Effect of systemic administration of lipopolysaccharides derived from Porphyromonas gingivalis on gene expression in mice kidney

Cited by 12 publications

References 27 publications

Periodontitis Exacerbates and Promotes the Progression of Chronic Kidney Disease Through Oral Flora, Cytokines, and Oxidative Stress

Periodontitis Exacerbates and Promotes the Progression of Chronic Kidney Disease Through Oral Flora, Cytokines, and Oxidative Stress

P. gingivalis Lipopolysaccharide Stimulates the Upregulated Expression of the Pancreatic Cancer-Related Genes Regenerating Islet-Derived 3 A/G in Mouse Pancreas

Melatonin improves periodontitis‐induced kidney damage by decreasing inflammatory stress and apoptosis in rats

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