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25-Hydroxy vitamin D3 modulates dendritic cell phenotype and function in Crohn's disease
Lars E Bartels1, Søren P Jørgensen, Mia Bendix
1Department of Medicine V (Hepatology and Gastroenterology), Gastro-Immuno Research Laboratory (GIRL), Aarhus University Hospital, Nørrebrogade 44, 8000 Aarhus, Denmark. larsbart@rm.dk
Inflammopharmacology
|January 24, 2013
Summary
Vitamin D (25-hydroxy vitamin D3) can modulate dendritic cell function in Crohn's disease (CrD) patients. This suggests vitamin D deficiency may contribute to CrD's inflammatory processes.
Area of Science:
- Immunology
- Endocrinology
- Gastroenterology
Background:
- Crohn's disease (CrD) involves an exaggerated immune response.
- Vitamin D's immunomodulatory effects are mediated by its activated form, 1,25-dihydroxy vitamin D3 (1,25-D3).
- Dendritic cells (DC) from healthy individuals activate 25-hydroxy vitamin D3 (25-D3).
Purpose of the Study:
- To investigate if DC from CrD patients can activate 25-D3.
- To determine if 25-D3 and 1,25-D3 modulate DC function in CrD patients.
Main Methods:
- Monocyte-derived DC from 20 CrD patients were cultured with 25-D3 or 1,25-D3 and lipopolysaccharide (LPS).
- DC surface marker expression, cytokine production, and allogeneic mixed leukocyte reaction were analyzed.
Main Results:
- 25-D3 and 1,25-D3 treatment reduced DC expression of CD80, CD83, CD86, and HLA-DR.
- TNF-α production was diminished, while CD14 and IL-6 production increased.
- Vitamin D3 treatment reduced DC's ability to activate lymphocytes.
Conclusions:
- DC from CrD patients intrinsically activate 25-D3.
- 25-D3 modulates DC function in CrD, reducing T cell activation.
- Vitamin D deficiency may contribute to CrD inflammation.
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