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Advanced glycation endproducts induce self- and cross-tolerance in monocytes

Introduction: Advanced glycation endproducts (AGEs) are well-known inflammatory mediators, which are recognized by immune cells through their corresponding receptor RAGE and have been shown to participate in the pathophysiology of a variety of acute as well as chronic inflammatory diseases. Neverthe...

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Main Authors: Uhle, Florian (Author) , Weiterer, Sebastian (Author) , Siegler, Benedikt Hermann (Author) , Brenner, Thorsten (Author) , Lichtenstern, Christoph (Author) , Weigand, Markus A. (Author)
Format: Article (Journal)
Language:English
Published: 28 June 2017
In: Inflammation research
Year: 2017, Volume: 66, Issue: 11, Pages: 961-968
ISSN:1420-908X
DOI:10.1007/s00011-017-1076-9
Online Access:Verlag, Pay-per-use, Volltext: http://dx.doi.org/10.1007/s00011-017-1076-9
Verlag, Pay-per-use, Volltext: https://doi.org/10.1007/s00011-017-1076-9
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Author Notes:Florian Uhle, Sebastian Weiterer, Benedikt Hermann Siegler, Thorsten Brenner, Christoph Lichtenstern, Markus Alexander Weigand

MARC

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520 |a Introduction: Advanced glycation endproducts (AGEs) are well-known inflammatory mediators, which are recognized by immune cells through their corresponding receptor RAGE and have been shown to participate in the pathophysiology of a variety of acute as well as chronic inflammatory diseases. Nevertheless, no data are available on the aftermath of AGE recognition on immune cells. Materials and methods: We used the monocytic cell line MonoMac6 as well as primary human monocytes for double stimulation experiments. We measured secreted as well as intracellular levels of TNF-α using ELISA and flow cytometry. In addition, gene expression of surface receptors (RAGE and TLR4) and TNF were measured by qPCR. Results: Stimulation with AGE leads to a dose-dependent induction of self- and cross-tolerance in both primary monocytes as well as the MonoMac6 cell line. The AGE tolerance depended neither on a decreased expression of RAGE or TLR4, nor on a decrease of TNF-α expression. Nevertheless, intracellular TNF-α was decreased, hinting towards a posttranscriptional regulation. Conclusion: High levels of AGEs are capable to activate immune cells at first, but induce a secondary state of hypo-responsiveness in these cells. Based on the origin of its causal agent, we propose this phenomenon to be “metabolic tolerance”. 
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