Vitamin D and Inflammatory Bowel Disease

Figure 1

Potential involvement of vitamin D in the pathogenesis of inflammatory bowel disease and immunologic effects of vitamin-D-related therapeutic approaches. Scenario A: reduced UV exposure as risk factor for CD and for hospitalizations and surgery [86]; Scenario B: NOD2 gene transcription is stimulated by 1,25(OH)₂D₃/VDR and signaling through NOD2 induces expression of DEFB2/HBD2 which stands for beta-defensin 2 and cathelicidin [20]; Scenarios C and D: variants or loss of function of VDR may lead to changes of the microbiota and reduce host defense by reducing production of cathelicidin, lysozyme, and ATG16L1 protein (autophagy) [21, 22]; Scenario E: experimental studies with vitamin D or its analogues showing inhibitory effects on PBMC, LPMC, dendritic cells, and fibroblasts in terms of cytokine production and differentiation (Table 3). VDR: vitamin D receptor; NOD: nucleotide-binding oligomerization domain.