Th17 and Treg lymphocytes in obesity and Type 2 diabetic patients

Wang, Mei; Chen, Fuqiong; Wang, Jingli; Zeng, Zhixuan; Yang, Qin; Shao, Shiying

doi:10.1016/j.clim.2018.09.005

Cited by 73 publications

(63 citation statements)

References 93 publications

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“…A diminished production of anti‐inflammatory factors such as interleukin‐4, interleukin‐10, transforming growth factor‐beta, and anti‐inflammatory lipid‐based mediators may potentially contribute to greater periodontal inflammation in diabetics . Several anti‐inflammatory cytokines are produced by regulatory T cells and M2 macrophages, both of which are reduced in many diabetic complications . Peroxisome proliferator‐activated receptor‐alpha, which has an anti‐inflammatory function, is suppressed in the periodontium of diabetic animals, and this reduction may potentially increase the level of inflammation …”

Section: Diabetes Periodontal Diseases and Inflammationmentioning

confidence: 99%

“…51,52 Several antiinflammatory cytokines are produced by regulatory T cells and M2 macrophages, both of which are reduced in many diabetic complications. [53][54][55] Peroxisome proliferator-activated receptor-alpha, which has an anti-inflammatory function, is suppressed in the periodontium of diabetic animals, and this reduction may potentially increase the level of inflammation. 56 An aspect of periodontitis that is likely to be important but which has not received as much attention is how the epithelial barrier is affected by diabetes.…”

Section: Iab E Te S Peri Odontal D Is E a S E S And Infl Ammamentioning

confidence: 99%

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The impact of diabetes on periodontal diseases

Graves

Ding

Yang

2019

Periodontology 2000

243

172

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The susceptibility and severity of periodontal diseases is made more severe by diabetes, with the impact on the disease process inversely proportional to the level of glycemic control. Although type 1 diabetes mellitus and type 2 diabetes mellitus have different etiologies, and their impact on bone is not identical, they share many of the same complications. Studies in animals and humans agree that both forms of diabetes increase inflammatory events in periodontal tissue, impair new bone formation, and increase expression of RANKL in response to bacterial challenge. High levels of glucose, reactive oxygen species, and advanced glycation end‐products are found in the periodontium of diabetic individuals and lead to increased activation of nuclear factor‐kappa B and expression of inflammatory cytokines such as tumor necrosis factor and interleukin‐1. Studies in animals, moreover, suggest that there are multiple cell types in periodontal tissues that are affected by diabetes, including leukocytes, vascular cells, mesenchymal stem cells, periodontal ligament fibroblasts, osteoblasts, and osteocytes. The etiology of periodontal disease involves the host response to bacterial challenge that is affected by diabetes, which increases the expression of RANKL and reduces coupled bone formation. In addition, the inflammatory response also modifies the oral microbiota to render it more pathogenic, as demonstrated by increased inflammation and bone loss in animals where bacteria are transferred from diabetic donors to germ‐free hosts compared with transfer from normoglycemic donors. This approach has the advantage of not relying upon limited knowledge of the specific bacterial taxa to determine pathogenicity, and examines the overall impact of the microbiota rather than the presumed pathogenicity of a few bacterial groups. Thus, animal studies have provided new insights into pathogenic mechanisms that identify cause‐and‐effect relationships that are difficult to perform in human studies.

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Section: Diabetes Periodontal Diseases and Inflammationmentioning

confidence: 99%

Section: Iab E Te S Peri Odontal D Is E a S E S And Infl Ammamentioning

confidence: 99%

The impact of diabetes on periodontal diseases

Graves

Ding

Yang

2019

Periodontology 2000

243

172

View full text Add to dashboard Cite

show abstract

“…A recent meta-analysis study revealed the potential mechanistic, diagnostic, and therapeutic implications of different classes of lipids in AD (Zarrouk et al, 2017 ). Obesity and diabetes present inflammatory components (Wang et al, 2018 ). Indeed, obese patients often display basal low-grade systemic inflammation in adipose tissue and increased susceptibility to immune-mediated diseases (Sun et al, 2012 ; Mraz and Haluzik, 2014 ).…”

Section: Crosstalk Between Peripheral Metabolic Diseases and Brain Pamentioning

confidence: 99%

Insulin Resistance in Alzheimer's Disease

et al. 2018

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The epidemiological connection between diabetes, obesity, and dementia represents an important public health challenge but also an opportunity to further understand these conditions. The key intersection among the three diseases is insulin resistance, which has been classically described to occur in peripheral tissues in diabetes and obesity and has recently been shown to develop in Alzheimer's disease (AD) brains. Here we review encouraging preclinical and clinical data indicating the potential of targeting impaired insulin signaling with antidiabetic drugs to treat dementia. We further discuss biological mechanisms through which peripheral metabolic dysregulation may lead to brain malfunction, providing possible explanations for the connection between diabetes, obesity, and AD. Finally, we briefly discuss how lifelong allostatic load may interact with aging to increase the risk of dementia in late life.

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“…Notably, over 90% of patients with T2D are obese [5] and these individuals present with ectopic lipid accumulation that is associated with adipose tissue (AT) dysfunction [6]. Although mechanisms involved in AT dysfunction in T2D are complex, enhanced infiltration of leukocytes into the AT promotes low-grade chronic inflammation which is mediated by T-helper (Th) 1 and Th17 responses [7]. Interestingly, our group and others have provided cumulative findings showing that persistent Th1 and Th17 cytokine levels which include tumor necrosis factor-α (TNFα), interleukin-1 (IL-1), IL-6 and IL-17 exacerbates insulin resistance which may ultimately lead to cardiovascular complications [8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Natural killer cell levels in adults living with type 2 diabetes: a systematic review and meta-analysis of clinical studies

et al. 2020

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Background Chronic immune activation and hyperglycaemia are a hallmark of type 2 diabetes mellitus (T2D) while natural killer (NK) cells are involved in the pathogenesis of T2D. Dysregulated NK cell responses are associated with an increased risk of cardiovascular disease in patients living with T2D. Objective To provide a comprehensive and systematic evidence-based estimate on the levels of NK cells in patients living with T2D. Results This systematic review and meta-analysis included 13 studies reporting on 491 adult patients with T2D and 1064 nondiabetic controls. The pooled effect estimates showed increased levels of NK cells in adult patients with T2D compared to controls (MD: 0.03 [− 3.20, 3.26], I2 = 97%, p < 0.00001). Conclusion Overall, the evidence presented in this systematic review shows that the changes in NK cells in patients living with T2D are still unclear and further studies are needed.

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Th17 and Treg lymphocytes in obesity and Type 2 diabetic patients

Cited by 73 publications

References 93 publications

The impact of diabetes on periodontal diseases

The impact of diabetes on periodontal diseases

Insulin Resistance in Alzheimer's Disease

Natural killer cell levels in adults living with type 2 diabetes: a systematic review and meta-analysis of clinical studies

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