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    Anti-Inflammatory Effects of Vitamin D on Human Immune Cells in the Context of Bacterial Infection

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    Author
    Hoe, E; Nathanielsz, J; Toh, ZQ; Spry, L; Marimla, R; Balloch, A; Mulholland, K; Licciardi, PV
    Date
    2016-12-01
    Source Title
    Nutrients
    Publisher
    MDPI
    University of Melbourne Author/s
    Mulholland, Edward
    Affiliation
    Paediatrics (RCH)
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Hoe, E., Nathanielsz, J., Toh, Z. Q., Spry, L., Marimla, R., Balloch, A., Mulholland, K. & Licciardi, P. V. (2016). Anti-Inflammatory Effects of Vitamin D on Human Immune Cells in the Context of Bacterial Infection. NUTRIENTS, 8 (12), https://doi.org/10.3390/nu8120806.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257571
    DOI
    10.3390/nu8120806
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5188461
    Abstract
    Vitamin D induces a diverse range of biological effects, including important functions in bone health, calcium homeostasis and, more recently, on immune function. The role of vitamin D during infection is of particular interest given data from epidemiological studies suggesting that vitamin D deficiency is associated with an increased risk of infection. Vitamin D has diverse immunomodulatory functions, although its role during bacterial infection remains unclear. In this study, we examined the effects of 1,25(OH)₂D₃, the active metabolite of vitamin D, on peripheral blood mononuclear cells (PBMCs) and purified immune cell subsets isolated from healthy adults following stimulation with the bacterial ligands heat-killed pneumococcal serotype 19F (HK19F) and lipopolysaccharide (LPS). We found that 1,25(OH)₂D₃ significantly reduced pro-inflammatory cytokines TNF-α, IFN-γ, and IL-1β as well as the chemokine IL-8 for both ligands (three- to 53-fold), while anti-inflammatory IL-10 was increased (two-fold, p = 0.016) in HK19F-stimulated monocytes. Levels of HK19F-specific IFN-γ were significantly higher (11.7-fold, p = 0.038) in vitamin D-insufficient adults (<50 nmol/L) compared to sufficient adults (>50 nmol/L). Vitamin D also shifted the pro-inflammatory/anti-inflammatory balance towards an anti-inflammatory phenotype and increased the CD14 expression on monocytes (p = 0.008) in response to LPS but not HK19F stimulation. These results suggest that 1,25(OH)₂D₃ may be an important regulator of the inflammatory response and supports further in vivo and clinical studies to confirm the potential benefits of vitamin D in this context.

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