Journal
INNATE IMMUNITY
Volume 28, Issue 3-4, Pages 138-151Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/17534259221097835
Keywords
soluble CD163; monocyte-derived macrophages; alveolar macrophages; idiopathic pulmonary fibrosis; biomarker
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Funding
- Institut National de la Sante et de la Recherche Medicale (INSERM)
- Universite de Rennes (Univ Rennes)
- Boehringer Ingelheim Pharma
- Roche
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This study found that M-MoDM and sCD163 levels in pulmonary tissues and alveolar fluids were elevated in IPF patients. However, serum sCD163 levels were not correlated with disease severity.
The soluble form of the membrane hemoglobin scavenger receptor CD163 (sCD163), released by shedding, is a strong marker for macrophage activation. Serum sCD163 levels rise in several acute inflammatory states and some fibrosing diseases. Monocyte-derived macrophages (MoDM) differentiated by macrophage colony-stimulating factor (M-MoDM) contribute to the pathophysiology of idiopathic pulmonary fibrosis (IPF), an irreversible and rapidly fatal interstitial lung disease. Since M-MoDM express high membrane CD163 levels, we thus postulated that sCD163 could be a relevant biomarker for macrophage activation in IPF. We found that M-MoDM constitutively released higher amounts of sCD163 (49.5 +/- 24.5 ng/ml) than monocytes (0.45 +/- 0.32 ng/ml) or MoDM differentiated with granulocyte macrophage-stimulating factor (2.24 +/- 0.98 ng/ml). The basal production of sCD163 by M-MoDM was increased following stimulation with lipopolysaccharide (123.4 +/- 54.9 ng/ml) or ATP (168.9 +/- 41.8 ng/ml). The sCD163 release was controlled by metalloproteases but not through ADAM17 activation. Moreover, CD163-positive macrophages and sCD163 were detected in pulmonary tissues and alveolar fluids of Caucasian patients with IPF, respectively. IPF alveolar macrophages constitutively secreted sCD163 amounts (67.6 +/- 44.6 ng/mu g RNA) which were significantly higher than those released by alveolar macrophages isolated from controls (19.2 +/- 7.6 ng/mu g RNA) or patients with other interstitial lung disease (31.5 +/- 16.6 ng/mu g RNA). However, the concentrations of sCD163 in blood serum collected from 155 patients with IPF did not correlate with the severity of their disease. In conclusion, our results show that M-MoDM constituted a pertinent model to study the regulation of sCD163 production. Yet, serum sCD163 values could not provide a prognostic biomarker for IPF in our cohort.
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