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Soluble CD163, a specific macrophage activation marker, is decreased by anti-TNF-α antibody treatment in active

A Dige1, S Støy, K L Thomsen

  • 1Gastro-Immuno Research Laboratory (GIRL), Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus C, Denmark; Department of Medicine, Horsens Regional Hospital, Horsens C, Denmark.

Scandinavian Journal of Immunology
|October 28, 2014
PubMed

Insights

Soluble CD163 (sCD163) indicates macrophage activation in Crohn's disease (CD) and ulcerative colitis (UC). Anti-TNF-α therapy rapidly reduced sCD163, unlike prednisolone, suggesting specific effects on macrophage activity in inflammatory bowel diseases.

Area of Science:

  • Immunology
  • Gastroenterology
  • Biomarker Discovery

Background:

  • Activated macrophages release soluble CD163 (sCD163), a scavenger receptor, into circulation.
  • sCD163 serves as a potential in vivo marker for macrophage activation.
  • Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), involve significant immune dysregulation and macrophage activation.

Purpose of the Study:

  • To measure sCD163 levels as a marker of macrophage activation in patients with CD and UC.
  • To evaluate the effect of anti-tumour necrosis factor-alpha (TNF-α) antibody and prednisolone treatments on sCD163 levels.
  • To investigate CD163 expression on circulating monocytes in patients with CD.

Main Methods:

  • Plasma sCD163 levels were measured in 58 CD patients, 40 UC patients, and 90 healthy controls (HC) at baseline and during 6 weeks of treatment.
  • Treatments included anti-TNF-α antibody or prednisolone.
  • CD163 expression on CD14(+) monocytes was assessed in 21 CD patients receiving anti-TNF-α therapy.

Main Results:

  • Baseline sCD163 levels were significantly elevated in both CD and UC patients compared to HC (P < 0.001).
  • Anti-TNF-α antibody treatment rapidly decreased sCD163 levels within 1 day (P < 0.05) and normalized them in UC patients.
  • Prednisolone treatment did not reduce sCD163 levels, and CD patients showed sustained elevated sCD163 despite anti-TNF-α therapy. Monocytic CD163 expression was increased in CD patients.

Conclusions:

  • Active CD and UC are associated with heightened macrophage activation, reflected by elevated sCD163 and monocytic CD163 expression.
  • Anti-TNF-α antibody treatment effectively reduces macrophage activation markers in IBD.
  • sCD163 serves as a sensitive biomarker for monitoring macrophage activation and treatment response in IBD.

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