scholarly journals Dietary Advanced Glycation Endproducts Induce an Inflammatory Response in Human Macrophages in Vitro

Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1868 ◽  
Author(s):  
Timme van der Lugt ◽  
Antje Weseler ◽  
Wouter Gebbink ◽  
Misha Vrolijk ◽  
Antoon Opperhuizen ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Human Health ◽  
Advanced Glycation Endproducts ◽  
Food Products ◽  
Tnf Alpha ◽  
Human Macrophage ◽  
Advanced Glycation ◽  
Glycation Endproducts ◽  
Rich Food

Advanced glycation endproducts (AGEs) can be found in protein- and sugar-rich food products processed at high temperatures, which make up a vast amount of the Western diet. The effect of AGE-rich food products on human health is not yet clear and controversy still exists due to possible contamination of samples with endotoxin and the use of endogenous formed AGEs. AGEs occur in food products, both as protein-bound and individual molecules. Which form exactly induces a pro-inflammatory effect is also unknown. In this study, we exposed human macrophage-like cells to dietary AGEs, both in a protein matrix and individual AGEs. It was ensured that all samples did not contain endotoxin concentrations > 0.06 EU/mL. The dietary AGEs induced TNF-alpha secretion of human macrophage-like cells. This effect was decreased by the addition of N(ε)-carboxymethyllysine (CML)-antibodies or a receptor for advanced glycation endproducts (RAGE) antagonist. None of the individual AGEs induce any TNF-alpha, indicating that AGEs should be bound to proteins to exert an inflammatory reaction. These findings show that dietary AGEs directly stimulate the inflammatory response of human innate immune cells and help us define the risk of regular consumption of AGE-rich food products on human health.

scholarly journals Dietary Advanced Glycation Endproducts Decrease Glucocorticoid Sensitivity In Vitro

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 441 ◽  
Author(s):  
Timme van der Lugt ◽  
Antje R. Weseler ◽  
Misha F. Vrolijk ◽  
Antoon Opperhuizen ◽  
Aalt Bast
Keyword(s):  
Inflammatory Response ◽  
Glucocorticoid Receptor ◽  
Advanced Glycation Endproducts ◽  
Food Products ◽  
Glucocorticoid Resistance ◽  
Human Macrophage ◽  
Advanced Glycation ◽  
Phosphorylation State ◽  
Glycation Endproducts ◽  
Anti Inflammatory

Glucocorticoids are very effective anti-inflammatory drugs and widely used for inflammatory bowel disease (IBD) patients. However, approximately 20% of IBD patients do not respond to glucocorticoids and the reason for this is largely unknown. Dietary advanced glycation endproducts (AGEs) are formed via the Maillard reaction during the thermal processing of food products and can induce a pro-inflammatory reaction in human cells. To investigate whether this pro-inflammatory response could be mitigated by glucocorticoids, human macrophage-like cells were exposed to both LPS and AGEs to induce interleukin-8 (IL8) secretion. This pro-inflammatory response was then modulated by adding pharmacological compounds interfering in different steps of the anti-inflammatory mechanism of glucocorticoids: rapamycin, quercetin, and theophylline. Additionally, intracellular reactive oxygen species (ROS) were measured and the glucocorticoid receptor phosphorylation state was assessed. The results show that AGEs induced glucocorticoid resistance, which could be mitigated by quercetin and rapamycin. No change in the phosphorylation state of the glucocorticoid receptor was observed. Additionally, intracellular ROS formation was induced by AGEs, which was mitigated by quercetin. This suggests that AGE-induced ROS is an underlying mechanism to AGE-induced glucocorticoid resistance. This study shows for the first time the phenomenon of dietary AGE-induced glucocorticoid resistance due to the formation of ROS. Our findings indicate that food products with a high inflammatory potential can induce glucocorticoid resistance; these results may be of great importance to IBD patients suffering from glucocorticoid resistance.

scholarly journals Gastrointestinal digestion of dietary advanced glycation endproducts using an in vitro model of the gastrointestinal tract (TIM-1)

2020 ◽  
Vol 11 (7) ◽  
pp. 6297-6307 ◽  
Author(s):  
Timme van der Lugt ◽  
Koen Venema ◽  
Stefan van Leeuwen ◽  
Misha F. Vrolijk ◽  
Antoon Opperhuizen ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
In Vitro Model ◽  
Advanced Glycation Endproducts ◽  
Food Products ◽  
Advanced Glycation ◽  
Gastrointestinal Digestion ◽  
Glycation Endproducts ◽  
Vitro Model

In a sophisticated gastrointestinal model, dietary advanced glycation endproducts (dAGEs) in food products remain bound to proteins after digestion and concentrations increase.

scholarly journals Gastrointestinal digestion of dietary advanced glycation endproducts increases their pro-inflammatory potential

2021 ◽  
Author(s):  
T. van der Lugt ◽  
M. F. Vrolijk ◽  
T. F. H. Bovee ◽  
S. P. J. van Leeuwen ◽  
S. Vonsovic ◽  
...  
Keyword(s):  
Advanced Glycation Endproducts ◽  
Advanced Glycation ◽  
Gastrointestinal Digestion ◽  
Glycation Endproducts

Digestion of dietary advanced glycation endproducts (dAGEs) increases its pro-inflammatory potential in vitro.

Phytochemicals as Potential Inhibitors of Advanced Glycation End Products: Health Aspects and Patent Survey

2021 ◽  
Vol 12 ◽  
Author(s):  
Annayara C. F. Fernandes ◽  
Jeane B. Melo ◽  
Vanize M. Genova ◽  
Ádina L. Santana ◽  
Gabriela Macedo
Keyword(s):  
Phenolic Compounds ◽  
Inflammatory Responses ◽  
Low Cost ◽  
Advanced Glycation Endproducts ◽  
Advanced Glycation ◽  
Glycation Endproducts ◽  
Synthetic Drugs ◽  
Peanut Skins

Background: Glycation is a chemical reaction that synthesize advanced glycation endproducts (AGEs). The AGEs irreversibly damage macromolecules present in tissues and organs, leading to the impairment of biological functions. For instance, the accumulation of AGEs induces oxidative stress and consequently inflammatory responses in human body, leading to the on set/worsening of diseases, including obesity, asthma, cognitive impairment, and cancer. There is a current demand on natural and low-cost sources of antiglycant agents. As a result, food phytochemicals presented promising results to inhibit glycation and consequently, the formation of AGEs. Objective: Here, we describe the mechanism of glycation on the worsening of diseases, the methods os detection, and the current findings on the use of phytochemicals (phenolic compounds, phytosterols, carotenoids, terpenes and vitamins) as natural therapeuticals to inhibit health damages via inhibition of AGEs in vitro and in vivo. Methods: This manuscript reviewed publications available in the PubMed and Science Direct databases dated from the last 20 years on the uses of phytochemicals to inhibit the AGEs in vitro and in vivo. Also, recent patents on the use of anti-glycant drugs were reviewed using the Google Advanced Patents database. Results and Discussion: Phenolic compounds have been mostly studied to inhibit AGEs. Food phytochemicals derived from agroindustry wastes, including peanut skins, and the bagasses derived from citrus and grapes are promising antiglycant agents via scavenging of free radicals, metal ions, the suppression of metabolic pathways that induces inflammation, the activation of pathways that promote antioxidant defense, the blocking of AGE connection with the receptor for advanced glycation endproducts (RAGE). Conclusion: Phytochemicals derived from agroindustry are promising anti-glycants, which can be included to replace synthetic drugs for AGE inhibition, and consequently to act as a therapeutical strategy to prevent and treat diseases caused by AGEs, including diabetes, ovarian cancer, osteoporosis, and Alzheimer’s disease.

scholarly journals Advanced glycation endproducts mediate pro-inflammatory actions in human gestational tissues via nuclear factor-κB and extracellular signal-regulated kinase 1/2

2007 ◽  
Vol 193 (2) ◽  
pp. 269-277 ◽  
Author(s):  
Martha Lappas ◽  
Michael Permezel ◽  
Gregory E Rice
Keyword(s):  
Oxidative Stress ◽  
Human Placenta ◽  
Advanced Glycation Endproducts ◽  
Nuclear Factor Κb ◽  
Mitogen Activated Protein Kinase ◽  
Nuclear Factor ◽  
Advanced Glycation ◽  
Glycation Endproducts ◽  
Gestational Tissues

Processes of human labour include increased oxidative stress, formation of inflammatory mediators (e.g. cytokines) and uterotonic phospholipid metabolites (e.g. prostaglandins). In non-gestational tissues, advanced glycation endproducts (AGE) induce the expression of pro-inflammatory molecules through mitogen-activated protein kinase and nuclear factor κB (NF-κB)-dependent pathways. Thus, the aim of this study was to investigate the effects of AGE on 8-isoprostane (a marker of oxidative stress), pro-inflammatory cytokine and prostaglandin release in human gestational tissues, and to define the signalling pathways involved. Human placenta and gestational membranes (amnion and choriodecidua combined; n=5) were incubated in the absence or presence of AGE–BSA (0.25, 0.5, 1 and 2 mg/ml) for 18 h. AGE significantly increased in vitro release of tumour necrosis factor-α, interleukin (IL)-1β, IL-6, IL-8, prostaglandin (PG)E2, PGF2α and 8-isoprostane from human placenta and gestational membranes. This was associated with a concomitant increase in NF-κB p65 activation and ERK 1/2 phosphorylation. AGE-stimulated 8-isoprostane, cytokine and prostaglandin production was significantly suppressed by the ERK 1/2 inhibitor U0126 and the NF-κB inhibitor BAY 11-7082. In conclusion, AGE mediates inflammatory actions in human gestational tissues. Protein kinases and the NF-κB pathway play an essential role in AGE signalling in human gestational tissues.

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