S100A9/CD163 expression profiles in classical monocytes as biomarkers to discriminate idiopathic pulmonary fibrosis from idiopathic nonspecific interstitial pneumonia
Open Access
- 9 June 2021
- journal article
- research article
- Published by Springer Science and Business Media LLC in Scientific Reports
- Vol. 11 (1), 1-8
- https://doi.org/10.1038/s41598-021-91407-9
Abstract
Circulating monocytes have pathogenic relevance in idiopathic pulmonary fibrosis (IPF). Here, we determined whether the cell surface levels of two markers, pro-inflammatory-related S100A9 and anti-inflammatory-related CD163, expressed on CD14strongCD16− classical monocytes by flow cytometry could discriminate IPF from idiopathic nonspecific interstitial pneumonia (iNSIP). Twenty-five patients with IPF, 25 with iNSIP, and 20 healthy volunteers were prospectively enrolled in this study. The S100A9+CD163− cell percentages in classical monocytes showed a pronounced decrease on monocytes in iNSIP compared to that in IPF. In contrast, the percentages of S100A9−CD163+ cells were significantly higher in iNSIP patients than in IPF patients and healthy volunteers. In IPF patients, there was a trend toward a correlation between the percentage of S100A9+CD163− monocytes and the surfactant protein-D (SP-D) serum levels (r = 0.4158, [95% confidence interval (CI) − 0.02042–0.7191], p = 0.051). The individual percentages of S100A9+CD163− and S100A9−CD163+ cells were also independently associated with IPF through multivariate regression analysis. The unadjusted area under the receiver operating characteristic curve (ROC-AUC) to discriminate IPF from iNSIP was (ROC-AUC 0.802, 95% CI [0.687–0.928]), suggesting that these are better biomarkers than serum SP-D (p < 0.05). This preliminary study reports the first comparative characterization of monocyte phenotypes between IPF and iNSIP.Funding Information
- JSPS KAKENHI Grant no. (JP16K08940, JP19K07894.)
This publication has 29 references indexed in Scilit:
- Reference values for spirometry, including vital capacity, in Japanese adults calculated with the LMS method and compared with previous valuesRespiratory Investigation, 2014
- Human S100A9 Protein Is Stabilized by Inflammatory Stimuli via the Formation of Proteolytically-Resistant HomodimersPLOS ONE, 2013
- Investigation of the freely available easy-to-use software ‘EZR’ for medical statisticsBone Marrow Transplantation, 2012
- S100A9 in BALF is a candidate biomarker of idiopathic pulmonary fibrosisRespiratory Medicine, 2012
- An Official ATS/ERS/JRS/ALAT Statement: Idiopathic Pulmonary Fibrosis: Evidence-based Guidelines for Diagnosis and ManagementAmerican Journal of Respiratory and Critical Care Medicine, 2011
- The endogenous Toll–like receptor 4 agonist S100A8/S100A9 (calprotectin) as innate amplifier of infection, autoimmunity, and cancerJournal of Leukocyte Biology, 2009
- Multidisciplinary interobserver agreement in the diagnosis of idiopathic pulmonary fibrosisEuropean Respiratory Journal, 2008
- Blood Monocytes Consist of Two Principal Subsets with Distinct Migratory PropertiesImmunity, 2003
- Oxygen Radical Production by Alveolar Inflammatory Cells in Idiopathic Pulmonary FibrosisAmerican Review of Respiratory Disease, 1990
- Measuring the Accuracy of Diagnostic SystemsScience, 1988