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Cited by 50Advanced Glycation End Products researchDialysis and Renal Disease ManagementImmune Response and Inflammation

Effect of advanced glycation end products on endotoxin-induced TNF-a, IL-1b and IL-8 in human peripheral blood mononuclear cells

Reznikov, L.L., Waksman, J., Azam, T., Kim, S.-H., Bufler, P., Niwa, T., Werman, A., Zhang, X. +3 more·2004·Clinical Nephrology
DOI 10.5414/cnp61324
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Abstract

BACKGROUND/AIMS: Advanced glycated end products (AGE) are endogenous proteins that have formed covalent complexes with sugars by a nonenzymatic process. Being proinflammatory molecules, AGE are thought to contribute to chronic systemic and local inflammatory processes associated with pathological changes in various diseases. In patients with end-stage renal disease, AGE are believed to play a role in the progression of atherosclerosis and worsening of renal failure. In patients receiving hemodialysis, AGE are thought to contribute to the inflammatory components of the therapy, particularly in diabetic patients. METHODS: In the present study, AGE were produced using 5% human serum albumin (HSA) and 50% glucose, both used for intravenous infusion into humans and both released after strict control for endotoxin content. The presence of AGE formed by HSA and glucose was confirmed using 2 independent assays. The inflammatory properties of these AGE were assessed using synthesis and release of the proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor (TNF) and IL-8, a chemokine. RESULTS: Alone, AGE did not induce these cytokines from peripheral blood mononuclear cells (PBMC) obtained from 14 healthy human donors. However, in the presence of 1 or 10 ng/ml of endotoxin, AGE augmented the production of IL-1 and TNF above that induced by endotoxin alone. Although the amount of augmentation of LPS-induced cytokines by AGE varied between the blood donors, the response was consistently observed and reached statistical significance. The augmentation of cytokine production was confirmed using AGE prepared with different lots of HSA and glucose. CONCLUSION: These results demonstrate that in the strict absence ofendotoxins, AGE are formed that do not stimulate cytokine production from PBMC of healthy donors, however, AGE significantly augment the synthesis and release of proinflammatory cytokine in the presence of low concentrations of endotoxins. The data suggest that renal replacement therapies should consider the role of microbial products in potentiating the biological consequences of naturally formed AGE and their potential to contribute to systemic and local inflammation in renal replacement therapies. Therefore, although the formation of AGE is unavoidable, excluding microbial products during renal replacement therapy should reduce the pathological consequences of AGE.

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  • In db/db mice, wound healing was accelerated by a low-advanced glycation end product diet, with predominant wound contraction, compared with a high-advanced glycation end product diet.

    “Finally, in db/db mice, wound healing was accelerated by a low-AGE diet, with predominant wound contraction, compared with animals on a high-AGE diet, which favoured the epithelialisation mode of wound closure (513) .”

    From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [513]

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Authors
Reznikov, L. L., Waksman, J., Azam, T., Kim, S.-H., Bufler, P., Niwa, T., Werman, A., Zhang, X., Pischetsrieder, M., Shaldon, S., & Dinarello, C. A.
Affiliations
University of Colorado Health (US)
ORCID
Venue
Clinical Nephrology
Publisher
Dustri-Verlgag Dr. Karl Feistle
Published
2004-05-01
Volume
61
Issue
05
Pages
324-336
ISSN
0301-0430 (ISSN-L)
DOI
10.5414/cnp61324
OpenAlex
W2322774045
Cited by
50
References
0
Citations by year
2025: 3 · 2023: 1 · 2022: 5 · 2021: 2 · 2020: 1 · 2019: 8 · 2017: 3 · 2016: 1 · 2015: 2 · 2014: 2 · 2013: 3 · 2012: 3
FWCI
1.88
Type
journal article
Language
en
Open access
closed
Locations
  • Clinical Nephrology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Heart, Lung, and Blood Institute (HL68743, P01HL068743)
  • National Cancer Institute (P30CA046934)
  • National Institute of Allergy and Infectious Diseases (AI‑15614)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
  • Health Sciences › Medicine › Nephrology › Dialysis and Renal Disease Management
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
advanced glycation end products, endotoxin, lipopolysaccharide, TNF-α, IL-1β, interleukin-8, inflammatory cytokines, peripheral blood mononuclear cells, inflammation, end-stage renal disease, hemodialysis, renal replacement therapy, human serum albumin, glucose
MeSH terms
Adult, Female, Humans, Interleukin-1, Leukocytes, Mononuclear, Lipopolysaccharides, Male, Middle Aged, Tumor Necrosis Factor-alpha, Interleukin-8, Glycation End Products, Advanced

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