Serum sCD163 as a biomarker of adipose tissue inflammation in obstructive sleep apnoea patients: limits and perspectives

From the author:

I thank D. Monneret and J-P. Bastard for their interest in our manuscript [1] and I could not agree more with their comment that the role of soluble CD163 (sCD163) in obstructive sleep apnoea (OSA) requires further detailed evaluation. As outlined in our article, the measurement of sCD163 in our patient cohort followed our results from the in vitro and in vivo studies demonstrating M1 polarisation of adipose tissue macrophages in response to intermittent hypoxia and thus, was not an a priori hypothesis of our study. Nonetheless, the detected independent association of sCD163 with OSA severity is intriguing.

CD163 is a haemoglobin scavenger receptor that is expressed by cells of the monocyte-M2-macrophage lineage [2]. The soluble form of CD163 is present in plasma of healthy individuals [3] but in response to several inflammatory mediators, levels rise acutely due to metalloproteinase-17/tumour necrosis factor-α-converting enzyme (ADAM17/TACE)-mediated cleavage [4–6]. sCD163 has emerged as a sensitive biomarker of inflammation and increased levels have been found in numerous pro-inflammatory conditions, i.e. sepsis, hepatitis, rheumatoid arthritis, scleroderma or atherosclerosis [7, 8]. Moreover, sCD163 is increasingly linked with adipose tissue inflammation and is considered a prognostic predictor for the development of type 2 diabetes [9–11]. Taken all this information together, sCD163 is a very attractive target in OSA.

In our cross-sectional study, univariate analysis revealed a significant correlation of sCD163 with all OSA severity parameters but also with body mass index and waist/hip ratio. However, in linear regression, adjusted for anthropometric and demographic parameters, the apnoea/hypopnoea index (AHI) (or oxygen desaturation index, when substituted for AHI) remained the only significant predictor of this response. Hence, these results along with the pre-clinical data generate the hypothesis that sCD163 may serve as a potential pro-inflammatory marker and predictor of metabolic consequences in OSA. However, testing this hypothesis, as acknowledged in our manuscript, warrants further targeted evaluation including large prospective studies.