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Liver myofibroblasts up-regulate monocyte CD163 expression via PGE2 during hepatitis B induced liver failure

Min Zhang, Yinong Ye, Fenglan Wang

  • 1Department of Infectious Diseases, The Third Affiliated Hospital of Sun Yat-sen University, No 600 Tianhe Road, Guangzhou 510630, Guangdong Province, People's Republic of China. ytchong2005@126.com.

Journal of Translational Medicine
|March 7, 2014
PubMed
Abstract

Insights

Liver myofibroblasts promote CD163 expression on monocytes in liver failure. This suggests myofibroblasts regulate monocyte function, impacting patient outcomes in hepatitis B induced liver failure.

Area of Science:

  • Immunology
  • Hepatology
  • Cell Biology

Background:

  • Liver failure is associated with an inflammatory imbalance.
  • Increased CD163 expression in liver failure correlates with poor outcomes.
  • Regulatory mechanisms of CD163 expression remain unclear.

Purpose of the Study:

  • Investigate the role of liver myofibroblasts in regulating CD163 expression on monocytes.
  • Determine the mechanism by which liver myofibroblasts influence CD163 expression.

Main Methods:

  • Assessed CD163 expression on monocytes from liver failure patients using flow cytometry.
  • Isolated human liver myofibroblasts and co-cultured with monocytes in vitro.
  • Measured prostaglandin E2 (PGE2) production and its effect on CD163 expression.

Main Results:

  • CD163+ monocytes were enriched in diseased livers and associated with myofibroblasts.
  • Liver myofibroblasts significantly induced CD163 expression on monocytes.
  • Myofibroblast-secreted PGE2 activated monocytes and increased CD163 expression, which was inhibited by NS-398.

Conclusions:

  • Liver myofibroblasts directly regulate CD163 expression on monocytes in hepatitis B induced liver failure.
  • Myofibroblast-derived PGE2 is a key mediator in this regulation.
  • These findings highlight a novel mechanism of monocyte function regulation in liver disease.

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