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Takashi Nouno, M. Okamoto, Koji Ohnishi, S. Kaieda, M. Tominaga, Yoshiaki Zaizen, M. Ichiki, S. Momosaki, Masayuki Nakamura, K. Fujimoto, J. Fukuoka, S. Shimizu, Y. Komohara, T. Hoshino (2019)
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N. Joshi, Satoshi Watanabe, Satoshi Watanabe, R. Verma, R. Jablonski, R. Jablonski, Ching‐I Chen, P. Cheresh, N. Markov, P. Reyfman, Alexandra McQuattie-Pimentel, L. Sichizya, Ziyan Lu, Raul Piseaux-Aillon, David Kirchenbuechler, A. Flozak, C. Gottardi, C. Cuda, H. Perlman, M. Jain, D. Kamp, G. Budinger, A. Misharin (2019)
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H. Møller, N. Peterslund, J. Graversen, S. Moestrup (2002)
Identification of the hemoglobin scavenger receptor/CD163 as a natural soluble protein in plasma.Blood, 99 1
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/µg RNA) which were significantly higher than those released by alveolar macrophages isolated from controls (19.2 ± 7.6 ng/µg RNA) or patients with other interstitial lung disease (31.5 ± 16.6 ng/µg 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.
Innate Immunity – SAGE
Published: Apr 1, 2022
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