Macrophages Play a Key Role in the Obesity‐Induced Periodontal Innate Immune Dysfunction via Nucleotide‐Binding Oligomerization Domain‐Like Receptor Protein 3 Pathway

Huang, Xiaohong; Takata, Yasuyuki; Ma, Chao; Wang, Yixiong; Xie, Baoyi; Xuan, Dongying; Zhang, Jincai

doi:10.1902/jop.2016.160102

Cited by 31 publications

(38 citation statements)

References 43 publications

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“…To investigate the possible interaction between periodontitis and chronic kidney disease in obesity, we induced periodontitis in mice of the high-fat diet-induced obesity (DIO) and control (low-fat diet) groups as reported in the previous studies (13,14). We observed whether the high-fat diet or periodontitis affected the levels of serum proteins as serum indicators of renal function (Table 1), and then we performed Student-Newman-Keuls (SNK) method for multiple comparisons.…”

Section: The High-fat Diet But Not Periodontitis Affects the Levels Omentioning

confidence: 99%

Periodontitis aggravates kidney damage in obese mice by MMP2 regulation

Chen¹,

Xuan²,

Zhang³

2018

BLL

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OBJECTIVE: To investigate the effect of periodontitis on the development of kidney damage in obese mice and its possible mechanism. METHODS: C57 BL/6J mice were fed high-fat (HF) or low-fat (LF) diet and then divided into four groups: obesity with periodontitis (HFP), obesity without periodontitis (HFC), normal mice with periodontitis (LFP) and normal mice without periodontitis (LFC). Serum indicators of renal function, namely serum total protein (TP), albumin (ALB), creatinine (Cr) and blood urea nitrogen (UREA) were measured. The histopathological examination of kidney tissues was performed. The expressions of transforming growth factor-β1 (TGF-β1), matrix metalloproteinase-2 (MMP2) and tissue inhibitors of metalloproteinases-1 (TIMP1) were detected by immunohistochemistry and real time RT-PCR. RESULTS: Obesity decreased TP and ALB, and increased serum Cr and UREA levels in normal and periodontitis mice groups, as well as induced glomerular and tubulointerstitial pathologic changes. Tubulointerstitial fi brosis was more severe in HFP group. In obese mice, periodontitis caused the downregulation of MMP2, and upregulation of TIMP1 and TGF-β1 at transcriptional and translational levels. CONCLUSIONS: In obese mice, periodontitis may aggravate pathological changes in the kidney. The possible mechanism might lie in downregulation of MMP2 and upregulation of MMP inhibitor, TIMP1, and Fig. 4, Ref. 16). Text in PDF www.elis.sk.

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Section: The High-fat Diet But Not Periodontitis Affects the Levels Omentioning

confidence: 99%

Periodontitis aggravates kidney damage in obese mice by MMP2 regulation

Chen¹,

Xuan²,

Zhang³

2018

BLL

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“…Obesity is a chronic inflammatory condition with worldwide prevalence, and numerous studies have described the impact of obesity in the pathophysiology of periodontal disease. Studies have reported that obesity is associated with greater prevalence and severity of disease aaa(Gorman, Kaye, Apovian, et al., ; Gorman, Kaye, Nunn, & Garcia, ; Jimenez, Hu, Marino, Li, & Joshipura, ; Linden, Patterson, Evans, & Kee, ), while mechanistic studies have revealed that macrophages exposed to a hyperlipidemic environment display altered functional capacity including reduced infiltration, activation and phagocytic capacity (Huang et al., ), defective oxidative burst (Lee et al., ; Mancuso et al., ) and decreased macrophage cytokine production (Chu et al., ; Doxey et al., ).…”

Section: Introductionmentioning

confidence: 99%

“…infiltration, activation and phagocytic capacity (Huang et al, 2012), defective oxidative burst (Lee et al, 1999;Mancuso et al, 2002) and decreased macrophage cytokine production (Chu et al, 1999;Doxey et al, 1998).…”

mentioning

confidence: 99%

Dysregulation of human miRNAs and increased prevalence of HHV miRNAs in obese periodontitis subjects

Naqvi

Brambila

Martínez

et al. 2019

J Clinic Periodontology

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Aim: To evaluate human and herpesvirus-encoded microRNA (miRNA) expression in healthy and diseased gingiva of obese and non-obese subjects and compare the impact of localized and systemic inflammation on human miRNA profiles. Material and methods: Healthy and inflamed gingival biopsies were collected from obese and non-obese subjects. Human and herpesvirus miRNA expression was quantified using quantitative PCR. Predicted targets of dysregulated miRNAs were identified using bioinformatics analysis, validated by dual luciferase assays and their expression assessed in healthy and diseased tissues. Results: Our results show differential expression of miRNAs in both diseased groups compared to healthy counterparts. MMP-16 is identified as a novel target of miRNAs altered in disease. Expression analysis of genes predicted as target of differentially expressed miRNAs show significant changes in disease compared with healthy tissues. Finally, quantitation of four herpesvirus derived viral miRNAs show that expression and prevalence of herpesvirus miRNAs in diseased gingiva of obese subjects. Conclusion: Our findings show that miRNA (both cellular and virus) expression are differentially responsive to local and systemic inflammation. Some of these miRNAs can modulate key cellular genes with direct consequences on inflammatory pathways suggesting their impact on oral tissue transcriptome and functions.

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“…77 Obesity also may abate the innate immune response in the periodontium, for example via attenuation of macrophage infiltration and activation. 78 This may explain the higher occurrence of spontaneous 79 and ligature-induced 80 periodontal breakdown in obese experimental animals.…”

Section: Ta B L E 4 (Continued)mentioning

confidence: 99%

Manifestations of systemic diseases and conditions that affect the periodontal attachment apparatus: Case definitions and diagnostic considerations

Albandar

Susin

Hughes

2018

J Clinic Periodontology

141

104

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This review identifies systemic diseases and conditions that can affect the periodontal attachment apparatus and cause loss of periodontal supporting tissues and, where possible, presents case definitions for these. Many of these diseases are associated with a profound loss of periodontal attachment and alveolar bone, and for some of these disorders the periodontal manifestations may be among the first signs of the disease. These case definitions may be useful in the early diagnosis of these diseases and may contribute to an improvement in the management of periodontal manifestations and improve the quality of life for these patients.

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Macrophages Play a Key Role in the Obesity‐Induced Periodontal Innate Immune Dysfunction via Nucleotide‐Binding Oligomerization Domain‐Like Receptor Protein 3 Pathway

Abstract: Obesity may paralyze innate immune response of periodontium via attenuating infiltration and activation of macrophages and further aggravate periodontal disease.

Cited by 31 publications

References 43 publications

Periodontitis aggravates kidney damage in obese mice by MMP2 regulation

Periodontitis aggravates kidney damage in obese mice by MMP2 regulation

Dysregulation of human miRNAs and increased prevalence of HHV miRNAs in obese periodontitis subjects

Manifestations of systemic diseases and conditions that affect the periodontal attachment apparatus: Case definitions and diagnostic considerations

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