Abstract
Vitamin D is a fat-soluble vitamin with multiple functions, including the modulation of the immune response, amongst others. Earlier studies have demonstrated that the active form of vitamin D, 1,25-dihydroxivitamin D, inhibits LPS-induced IL-6 and TNF-α production by human monocytes in a dose-dependent manner. On the other hand, some in vitro studies support that this vitamin has immune modulatory effects on viral infections. However, it remains unclear whether vitamin D regulates the immune response in infectious diseases triggered by viruses such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes COVID-19. This study aimed to evaluate the anti-inflammatory properties of vitamin D against the spike protein of the SARS-CoV-2 virus. For this purpose, vitamin D was used in two different doses of 10 and 25 nM on the THP-1 cell line, which was stimulated with low doses of the SARS-CoV-2 virus spike protein. The THP-1 cell line, which is derived from human monocytic cells, was chosen since it contains the ACE2 transporter of the spike protein. Moreover, it is a widely used model to examine inflammatory processes due to its potential to stimulate inflammation and the release of inflammatory cytokines. The THP-1 cells were incubated for 1 h with the spike protein, subsequently treated with the two selected doses of vitamin D and incubated for 24 h. ELISA and RT-qPCR techniques were used to quantify the levels of inflammatory cytokines. Our results showed that vitamin D had no effect on the mRNA transcriptional levels of cytokine IL-6, but it was able to down-regulate the transcriptional levels of the pro-inflammatory cytokines IL-1β and TNF-α. There was no dose–response relationship between vitamin D and the expression of these genes. In conclusion, vitamin D inhibited inflammatory cytokine production on spike protein-stimulated inflammation in the THP1 cell line. The study is being completed by testing higher doses of vitamin D and of the spike protein. Additionally, other markers of inflammation are being measured through the use of transcriptomic analyses of the control vs. treated THP1 cells.
Author Contributions
Conceptualization, E.M.-M., J.P., N.M.R.-M. and Á.A.-S.; methodology, Á.A.-S. and N.M.R.-M.; formal analysis, Á.A.-S. and N.M.R.-M.; investigation, Á.A.-S., N.M.R.-M., J.P. and E.M.-M.; resources, Á.A.-S. and N.M.R.-M.; writing—original draft preparation, Á.A.-S.; writing—review and editing, E.M.-M., J.P., N.M.R.-M.; supervision, E.M.-M. and J.P.; project administration, E.M.-M.; funding acquisition, E.M.-M. All authors have read and agreed to the published version of the manuscript.
Funding
This research was funded by Project PECOVID-0200-2020, funded by Consejería de Salud y Consumo de la Junta de Andalucía and cofunded by the European Regional Development Fund (ERDF-FEDER).
Data Availability Statement
This research was conducted using experimental data. Data can be obtained upon contacting the researchers.
Conflicts of Interest
The authors declare no conflict of interest.
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