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Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis
10:23

Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis

Published on: April 17, 2017

Effect of chronic hepatitis C virus infection on inflammatory lipid mediators

Cristina Tosti Guerra1, Patrizio Caini, Carlo Giannini

  • 1Department of Internal Medicine, Center for the Study of Systemic Manifestations of Hepatitis Viruses MaSVE, University of Florence, Florence, Italy.

Digestive and Liver Disease : Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
|December 6, 2007
PubMed

Insights

Chronic Hepatitis C virus (HCV) infection significantly decreases plasma platelet-activating factor acetylhydrolase (pPAF-AH) activity, increasing inflammation. pPAF-AH activity recovers only after successful HCV clearance.

Area of Science:

  • Immunology
  • Hepatology
  • Vascular Biology

Background:

  • Platelet-activating factor (PAF) is a key inflammatory mediator degraded by plasma PAF-acetylhydrolase (pPAF-AH).
  • Hepatitis C virus (HCV) is associated with serum lipoproteins, similar to pPAF-AH.
  • Reduced pPAF-AH activity is noted in various diseases, including systemic vasculitis.

Purpose of the Study:

  • To investigate the impact of chronic Hepatitis C virus (HCV) infection on the physiological functions of pPAF-AH.
  • To determine if HCV alters the PAF/pPAF-AH system.

Main Methods:

  • Studied 145 subjects: 56 HCV-infected, 52 HBV-infected (controls), and 37 healthy controls.
  • Measured plasma pPAF-AH activity, PAF levels, and Apo B100 titers.
  • Assessed pPAF-AH expression in macrophages and detected HCV-RNA in various tissues.

Main Results:

  • HCV patients exhibited elevated PAF levels and significantly reduced pPAF-AH activity.
  • pPAF-AH activity normalized in patients who cleared HCV post-treatment.
  • No significant changes in pPAF-AH mRNA expression or Apo B100 titers were observed in HCV patients.

Conclusions:

  • Chronic HCV infection appears to disrupt the PAF/pPAF-AH system.
  • This disruption may contribute to vascular damage associated with HCV.
  • Further research is warranted to explore the therapeutic implications of modulating the PAF/pPAF-AH system in HCV.
Abstract

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