Advanced glycation end products upregulate C-reactive protein synthesis by human hepatocytes through stimulation of monocyte IL-6 and IL-1 beta production.

Advanced glycation end products upregulate C-reactive protein synthesis by human hepatocytes through stimulation of monocyte IL-6 and IL-1 beta production. Research Abstract Details 

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Advanced glycation end products upregulate C-reactive protein synthesis by human hepatocytes through stimulation of monocyte IL-6 and IL-1 beta production. Abstract Text:

J -T Li,F -F Hou,Z -J Guo,Y -X Shan,X Zhang,Z -Q Liu,J -T Li,F -F Hou,Z -J Guo,Y -X Shan,X Zhang,Z -Q Liu,

Patients with chronic renal failure are characterized by increased plasma levels of C-reactive protein (CRP) and advanced glycation end products (AGE). AGE have been identified as a class of proinflammator mediators. To investigate whether AGE can stimulate hepatocytes to produce CRP, primary human fetal hepatocytes (HFH) were incubated with AGE-modified human serum albumin (AGE-HSA) or conditioned medium from AGE-HSA-stimulated monocytes (AGE-MCM). CRP concentrations in the supernatants were determined by an ELISA and CRP mRNA levels were determined by a quantitative RT-PCR. Exposure of HFH with AGE-HSA for 12-72 h did not change CRP concentrations in the supernatants. CRP protein and mRNA expression were significantly upregulated in a time- and dose-dependent manner when HFH were incubated with AGE-MCM. This stimulating effect was partially inhibited when AGE-MCM were preincubated with antibodies against interleukin-6 (anti-IL-6), interleukin-1 beta (anti-IL-1 beta), or soluble IL-1 receptor and was completely inhibited when AGE-MCM were preincubated with anti-IL-6 and anti-IL-1 beta simultaneously. The inhibiting effect did not occur when AGE-MCM was preincubated with antibody of tumour necrosis factor-alpha (anti-TNF-alpha) and soluble TNF receptor. Exposure of HFH with exogenous IL-6 and IL-1 beta, at the same concentrations as contained in AGE-MCM, also increased CRP production, but exogenous TNF-alpha had no effect. These results suggest that AGE cannot directly stimulate hepatocytes to produce CRP, but rather indirectly enhance CRP expression via stimulation of IL-6 and IL-1 beta production by human monocytes.

Advanced glycation end products upregulate C-reactive protein synthesis by human hepatocytes through stimulation of monocyte IL-6 and IL-1 beta production. Publishing Authors By Initials

JT Li,FF Hou,ZJ Guo,YX Shan,X Zhang,ZQ Liu,JT Li,FF Hou,ZJ Guo,YX Shan,X Zhang,ZQ Liu,

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Advanced glycation end products upregulate C-reactive protein synthesis by human hepatocytes through stimulation of monocyte IL-6 and IL-1 beta production. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Scandinavian journal of immunology

VOLUME: 66

Page Numbers: 555-62

Journal Abbreviation: Scand. J. Immunol.

ISSN: 0300-9475

DAY: 16

MONTH: Nov

YEAR: 2007

Advanced glycation end products upregulate C-reactive protein synthesis by human hepatocytes through stimulation of monocyte IL-6 and IL-1 beta production. Information

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LANGUAGE: eng

NlmUniqueID: 323767

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Grant and Affiliation Information for Advanced glycation end products upregulate C-reactive protein synthesis by human hepatocytes through stimulation of monocyte IL-6 and IL-1 beta production.

AFFILIATION: Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Country: England

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MEDLINETA: Scand J Immunol

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