Vitamin D represses rhinovirus replication in cystic fibrosis cells by inducing LL-37.
Schögler. Aline A; Muster. Ricardo J RJ; Kieninger. Elisabeth E; Casaulta. Carmen C; Tapparel. Caroline C; Jung. Andreas A; Moeller. Alexander A; Geiser. Thomas T; Regamey. Nicolas N; Alves. Marco P MP
Key Findings
- Vitamin D reduced rhinovirus load in CF bronchial cells in a dose‑dependent way
- Vitamin D increased LL‑37 expression up to ~17‑fold
- Adding LL‑37 directly lowered viral replication about 4‑fold
- Higher LL‑37 levels in patient samples correlated with lower viral loads
Practical Outcomes
- Maintaining adequate vitamin D status may boost LL‑37 production and help curb rhinovirus infections, particularly in cystic fibrosis. Biohackers can consider regular vitamin D supplementation to support innate immunity, but specific dosing for antiviral effects isn’t established yet. Clinical trials are needed to confirm benefits and optimal vitamin D levels for virus protection.
Summary
Vitamin D can lower the amount of common cold virus (rhinovirus) that infects lung cells from cystic fibrosis patients by boosting the body’s own antimicrobial peptide called LL‑37. The study showed that more vitamin D led to higher LL‑37 levels, and adding LL‑37 directly also cut the virus’s replication. This suggests that keeping vitamin D levels sufficient might help the immune system fight viral lung infections, especially for people with cystic fibrosis, though real‑world dosing still needs testing.
Abstract
Vitamin D has immunomodulatory properties in the defence against pathogens. Its insufficiency is a widespread feature of cystic fibrosis (CF) patients, which are repeatedly suffering from rhinovirus (RV)-induced pulmonary exacerbations.To investigate whether vitamin D has antiviral activity, primary bronchial epithelial cells from CF children were pre-treated with vitamin D and infected with RV16. Antiviral and anti-inflammatory activity of vitamin D was assessed. RV and LL-37 levels were measured in bronchoalveolar lavage (BAL) of CF children infected with RV.Vitamin D reduced RV16 load in a dose-dependent manner in CF cells (10(-7 )M, p<0.01). The antiviral response mediated by interferons remained unchanged by vitamin D in CF cells. Vitamin D did not exert anti-inflammatory properties in RV-infected CF cells. Vitamin D increased the expression of the antimicrobial peptide LL-37 up to 17.4-fold (p<0.05). Addition of exogenous LL-37 decreased viral replication by 4.4-fold in CF cells (p<0.05). An inverse correlation between viral load and LL-37 levels in CF BAL (r=-0.48, p<0.05) was observed.RV replication in primary CF bronchial cells was reduced by vitamin D through the induction of LL-37. Clinical studies are needed to determine the importance of an adequate control of vitamin D for prevention of virus-induced pulmonary CF exacerbations.
Study Information
pubmed
2015
2015-11-19T00:00:00.000Z
10.1183/13993003.00665-2015
73
49