The Distinct Regulation of the Vitamin D and Aryl Hydrocarbon Receptors in COVID-19

Author:

Robak Oliver1ORCID,Kastner Marie-Theres1,Voill-Glaninger Astrid2,Viveiros André2ORCID,Steininger Christoph13ORCID

Affiliation:

1. Department of Internal Medicine I, Medical University of Vienna, 1090 Vienna, Austria

2. Department of Laboratory Medicine, Klinik Landstraße, 1030 Vienna, Austria

3. Karl-Landsteiner Institute for Microbiome Research, Medical University of Vienna, 1090 Vienna, Austria

Abstract

(1) Background: SARS-CoV-2 affects several immune pathways, including the vitamin D (VDR) and the aryl hydrocarbon receptor pathways (AhR). The aim of the study was the evaluation of the VDR and AhR pathways in the blood of COVID-19 patients with regard to the severity of disease. (2) Methods: Observational, single-center, case–control design. A total of 240 samples were selected for exploration. Patients who tested negative for SARS-CoV-2 but suffered from other respiratory infections (ORIs) served as a control group. (3) Results: VDR-specific mRNA in the blood of patients with mild symptoms (131.2 ± 198.6) was significantly upregulated relative to the VDR expression of the ORI group (23.24 ± 42.60; p < 0.0001); however, VDR expression of critically ill patients showed an impaired upregulation (54.73 ± 68.34; p < 0.001). CYP27B1 expression was not significantly regulated during SARS-CoV-2 infection. There was a downregulation of VDR and CYP27B1 compared to survivors. There was no significant difference in 25(OH)-vitamin D3 levels between critically ill patients with regard to survival (24.3 ± 9.4 vs. 27.1 ± 11.3; p = 0.433). (4) Conclusion: The VDR and AhR pathways are distinctively regulated in patients suffering from COVID-19 depending on the severity of disease. A combination treatment of antiviral drugs and vitamin D substitution should be evaluated for potentially improved prognosis in COVID-19.

Funder

Medical-Scientific Fund of the Mayor of the Federal Capital Vienna

Austrian Science Fund

Publisher

MDPI AG

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