Dietary Vitamin D Mitigates Coronavirus-Induced Lung Inflammation and Damage in Mice
Gabriel Campolina-Silva, Ana Cláudia Dos Santos Pereira Andrade, Manoela Couto, Paloma G Bittencourt-Silva, Celso M Queiroz-Junior, Larisse De Souza B Lacerda, Ian De Meira Chaves, Leonardo C De Oliveira, Fernanda Martins Marim, Cleida A Oliveira, Glauber S F Da Silva, Mauro Martins Teixeira, Vivian Vasconcelos Costa
Viruses, doi:10.3390/v15122434
The COVID-19 pandemic caused by the SARS-CoV-2 (β-CoV) betacoronavirus has posed a significant threat to global health. Despite the availability of vaccines, the virus continues to spread, and there is a need for alternative strategies to alleviate its impact. Vitamin D, a secosteroid hormone best known for its role in bone health, exhibits immunomodulatory effects in certain viral infections. Here, we have shown that bioactive vitamin D (calcitriol) limits in vitro replication of SARS-CoV-2 and murine coronaviruses MHV-3 and MHV-A59. Comparative studies involving wild-type mice intranasally infected with MHV-3, a model for studying β-CoV respiratory infections, confirmed the protective effect of vitamin D in vivo. Accordingly, mice fed a standard diet rapidly succumbed to MHV-3 infection, whereas those on a vitamin D-rich diet (10,000 IU of Vitamin D 3 /kg) displayed increased resistance to acute respiratory damage and systemic complications. Consistent with these findings, the vitamin D-supplemented group exhibited lower viral titers in their lungs and reduced levels of TNF, IL-6, IL-1β, and IFN-γ, alongside an enhanced type I interferon response. Altogether, our findings suggest vitamin D supplementation ameliorates β-CoV-triggered respiratory illness and systemic complications in mice, likely via modulation of the host's immune response to the virus.
by MHV-3. While these findings open promising avenues for further exploration and emphasize the importance of continued research in this area, it is imperative for future studies to broaden the scope of this study by encompassing in vivo infection with SARS-CoV-2. This imperative step will provide a more comprehensive understanding of vitamin D's prospects in addressing COVID-19. As result, we argue that our findings should not be construed in the context of the current clinical landscape of studies on vitamin D and COVID-19. Instead, they may serve as a springboard for future preclinical research aimed at exploring the intricate relationship between Vitamin D and β-CoV infections.
Supplementary Materials: The following supporting information can be downloaded at: https:// www.mdpi.com/article/10.3390/v15122434/s1, Figure S1 and Raw data_Figures 1-6. Informed Consent Statement: Not applicable.
Conflicts of Interest: The authors declare no conflict of interest.
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'abstract': '<jats:p>The COVID-19 pandemic caused by the SARS-CoV-2 (β-CoV) betacoronavirus has posed a '
'significant threat to global health. Despite the availability of vaccines, the virus '
'continues to spread, and there is a need for alternative strategies to alleviate its impact. '
'Vitamin D, a secosteroid hormone best known for its role in bone health, exhibits '
'immunomodulatory effects in certain viral infections. Here, we have shown that bioactive '
'vitamin D (calcitriol) limits in vitro replication of SARS-CoV-2 and murine coronaviruses '
'MHV-3 and MHV-A59. Comparative studies involving wild-type mice intranasally infected with '
'MHV-3, a model for studying β-CoV respiratory infections, confirmed the protective effect of '
'vitamin D in vivo. Accordingly, mice fed a standard diet rapidly succumbed to MHV-3 '
'infection, whereas those on a vitamin D-rich diet (10,000 IU of Vitamin D3/kg) displayed '
'increased resistance to acute respiratory damage and systemic complications. Consistent with '
'these findings, the vitamin D-supplemented group exhibited lower viral titers in their lungs '
'and reduced levels of TNF, IL-6, IL-1β, and IFN-γ, alongside an enhanced type I interferon '
'response. Altogether, our findings suggest vitamin D supplementation ameliorates '
'β-CoV-triggered respiratory illness and systemic complications in mice, likely via modulation '
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