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Related Experiment Video

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Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein

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C-reactive protein modulates lipid mediators in a pro-inflammatory direction.

Makoto Kurano^1,2,3, Kazuhisa Tsukamoto^4,5, Hideaki Isago⁶

¹Department of Clinical Laboratory Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan. kurano-tky@umin.ac.jp.

Journal of Inflammation (London, England)

|August 13, 2025

Summary

C-reactive protein (CRP) influences atherosclerosis by altering bioactive lipid mediators. This study found CRP increases pro-inflammatory lipids and decreases anti-inflammatory ones, potentially driving disease progression.

Keywords:

C-reactive protein Eicosanoids Inflammation Lysophospholipids W3-fatty acid mediators

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Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein

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Published on: October 12, 2017

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Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

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Published on: September 15, 2017

Area of Science:

Biochemistry
Immunology
Cardiovascular Research

Background:

C-reactive protein (CRP) is a known risk factor for atherosclerosis.
While inflammation may confound this association, CRP itself is suspected of having pro-atherosclerotic and pro-inflammatory roles.

Purpose of the Study:

To investigate the mechanisms by which CRP modulates bioactive lipid mediators.
To understand CRP's role in lipid metabolism and inflammation relevant to atherosclerosis.

Main Methods:

Overexpression of human CRP in mice and HepG2 cells.
Analysis of cytokine levels (IL-6, TNF-a) in plasma and cell culture.
Comprehensive lipidomics analysis of plasma samples.
Investigation of CRP's binding interactions with specific lipid mediators.

Main Results:

CRP overexpression elevated plasma IL-6 and TNF-a levels in mice.
CRP increased plasma levels of lysophospholipids and sphingosine 1-phosphate.
CRP promoted pro-inflammatory lipid mediators (e.g., PGE2, LTA4 metabolites) while reducing anti-inflammatory ones (EPA, DHA derivatives).
CRP was found to bind directly to mediators like sphingosine 1-phosphate, PGE2, and PGF2a.

Conclusions:

CRP modulates lysophospholipids and eicosanoids.
These modulations appear to be in pro-atherosclerotic and pro-inflammatory directions.
CRP may directly influence lipid mediator pathways contributing to atherosclerosis.