Dig Dis Sci: Vitamin D deficiency leads to the activation of the colon's local renin-angionein system and exacerbates colon inflammation

Inflammatory bowel disease (IBD) is a chronic disease of the human gastrointestinal tract and consists of Crohn's disease (CD) and ulcerative colitis (UC).
the cause of IBD is still uncertain, the disorders that cause complex interactions between genetic, environmental, microbial and immune factors have been recognized.
the intestinal cortical barrier consists of cell-to-cell connections between single-layered endocyste cells and adjacent cells to prevent harmful substances, microorganisms, toxins and in-cavity antigens from entering the body.
damage or dissonance of the endosthal cortical connection and/or excessive apoptosis of the endocrine can impair barrier function, causing intracellular antigens and bacteria to shift to the intrinsic layer and triggering colon inflammation.
-angiosin system (RAS) can play a variety of physiological roles.
nephrine is a protease that splits angiotensin (AGT) into angiotensin (Ang)I and then into Angus II by angiotensin-converting enzyme (ACE), the main effect of RAS, which works in combination with angiotensin-receiving (AT1R and AT2R).
RAS components are also present in exoplasm tissues and may regulate local function through side secretion/self-secretion mechanisms.
interesting is that local colon RAS in patients with IBD is activated and may be involved in the promotion of colon inflammation.
vitamin D has a wide range of biological functions, including calcification and non-calcification activity, and symptoms of vitamin D deficiency are common in IBD patients.
vitamin D deficiency is associated with increased activity in IBD disease.
recent studies have shown that vitamin D inhibits colon inflammation by blocking excess mucosa epithelocyte apoptosis and protecting the colon mucosa barrier.
, the study aims to explore whether vitamin D inhibits local colon RAS activation to reduce inflammation of the colon mucous membranes in mouse models of colitis.
researchers used 2,4,6-trinitrobenzene sulfonate (TNBS)-induced C57BL / 6 mice fed vitamin D deficiency (VDD) for 8 weeks to build a colitis model to feed mice on a vitamin D-adequate (VDS) diet.
the severity of colitis through histology and quantifying inflammatory cytokines, RAS compositions and signaling pathps with real-time RT-PCR and Western imprinting.
study found a significant decrease in serum 25 (OH) D3 concentrations in mice fed VDD compared to mice fed VDS.
when these VDD mice were induced by TNBS to colonitis, they showed more severe colon inflammation than their VDS counterparts.
VDD feeding leads to higher mucosal inflammatory cytokine production, higher creatinine light-chain kinase tightly linked regulatory pathway activation and increased mucosal permeability are more severe.
VDD diet also enhances colon RAS activation.
treatment of chlorosatan, an angiotensin II blocker, significantly reduced colitis in TNBS-induced VDD mice.
this study confirms that vitamin D deficiency can lead to excessive activeness of local RAS in the colon and promote colon inflammation.