Association of serum deiodinase type 2 level with chronic obstructive pulmonary disease in the Polish population
AbstractBackgrounds: Deiodinase type 2 (DIO2) is a selenoenzyme involved in the synthesis of thyroid hormones. Chemerin is a newly investigated adipokine known also as novel chemokine. Both molecules have been recently expected and found to play an important role in inflammation and immunity. DIO2, for example, is upregulated during acute and chronic inflammation. In addition, inflammation-induced expression of DIO2 in macrophages has been confirmed, while chemerin modulates the activation and chemotaxis of immune cells. It is widely known that chronic obstructive pulmonary disease (COPD) – the most common lung disease in the world – is accompanied by an inflammatory process and immune activation. There are no studies demonstrating an association between DIO2, chemerin and COPD. The aim of this study was to estimate DIO2 and chemerin concentration in serum collected from patients suffering from COPD and to compare it with healthy subjects, as well as to correlate with basic and clinical characteristics. Methods: The study group included 50 patients with COPD and 30 healthy subjects. DIO2 and chemerin serum levels as well as c-reactive protein levels were determined in all the subjects using commercial enzyme-linked immunosorbent assay kits. The association between serum DIO2 and chemerin with sociodemographic and clinical variables was assessed. Results: DIO2 serum levels were significantly higher in the patients with COPD as compared to the control group (50.3±23.2 U/L vs. 13.3±13.1; p<0.00001). No differences were observed in serum chemerin levels between the patients and controls (107.559±86.695.6 vs. 100.701±53.805; p=0.54). Furthermore, there was no association between DIO2 and chemerin levels and other variables, and no correlation between both molecules. Conclusions: This study demonstrated that DIO2 levels were higher in the patients with COPD than in the control subjects. The examined molecules should be further investigated if they are intended to be considered markers of processes involved in COPD mechanisms.
Copyright (c) 2019 Elżbieta Gałecka, Anna Kumor-Kisielewska, Paweł Górski
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