bowel

Vitamin D Supplementation Positively Impacts GI Diseases?

It is well known that vitamin D positively influences human health, but data on its impact on the human gut microbiome are lacking. Researchers conducted a pilot study on sixteen healthy volunteers. They were endoscopically examined to access a total of 7 sites to investigate the effects of oral vitamin D3 supplementation on the human mucosa-associated and stool microbiome, as well as CD8(+) T cells. Supplementation decreased relative abundance of Gammaproteobacteria including Pseudomonas spp. and Escherichia/Shigella spp. and increased bacterial richness. While no major changes occurred in the terminal ileum, appendiceal orifice, ascending colon, and sigmoid colon or in stools, the CD8(+) T cell fraction was significantly increased in the terminal ileum. Researchers concluded vitamin D3 modulates the gut microbiome of the upper GI tract, which might explain its positive influence on GI diseases such as inflammatory bowel disease or bacterial infections, and local effects of vitamin D demonstrate pronounced regional differences in the response of the GI microbiome to external factors.

Bashir M, et al. Effects of high djoses of vitamin D3 on mucosa-associated gut microbiome vary between regions of the human gastrointestinal tract. Eur J Nutr. 2016;55(4): 1479-89. doi: 10.1007/s00394-015-0966-2. Epub 2015 Jul 1.

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Gluten Sensitivity and Neurological Disorders – From Gut to Brain!

Gluten sensitivity (GS) may be defined as a state of heightened immunological responsiveness in genetically susceptible people. This definition does not imply bowel involvement. The authors, all affiliated with the Department of Neurology at The Royal Hallamshire Hospital, Sheffield, UK, suggest that regarding GS as principally a disease of the small bowel is a historical misconception. They state that GS can be primarily, and at times exclusively a neurological disease, and that IgG antigliadin antibody should be part of the routine investigation of all patients with neurological dysfunction of obscure aetiology, particularly patients with ataxia and peripheral neuropathy. Statistical evidence showed that patients with neurological disease of unknown aetiology were found to have a much higher prevalence of circulating antigliadin antibodies (57%) in their blood than either healthy controls (12%) or those with neurological disorders of known aetiology (5%). More celiac disease (CD) specific serological markers such as anti-endomysium and transglutaminase antibodies may have helped in diagnosing CD, but their sensitivity as markers of other manifestation of GS (where the bowel is not affected) is low. Early diagnosis and removal of the trigger factor by the introduction of a gluten-free diet may be the most promising therapeutic intervention.

Hadjivassiliou M, et al. Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatry 2002 72:560-563. Published by group.bmj.com

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Lactobacillus acidophilus, immune regulation and colitis!

Intestinal immune regulatory signals govern gut homeostasis and is tightly controlled by the interaction of gut microbial gene products with pattern recognition receptors. The breakdown of such regulatory mechanisms may result in inflammatory bowel disease (IBD). Lactobacillus acidophilus contains unique surface layer proteins (Slps), including SlpA, SlpB, SlpX and lipoteichoic acid (LTA), which interact with pattern recognition receptors to mobilize immune responses. To demonstrate the role of SlpA in protective immune regulation, a strain of Lactobacillus acidophilus which solely expressed SlpA was generated. They demonstrated that its purified SlpA bind to the C-type lectin SIGNR3 to exert regulatory signals that result in mitigation of colitis, maintenance of healthy gastrointestinal microbiota, and protected gut mucosal barrier function. Interestingly, such protection was not observed in Slgnr3-/- mice, suggesting that the SlpA/SIGNR3 interaction plays a key regulatory role in colitis.

Lightfoot YL, et al. SIGNR3-dependent immune regulation by Lactobacillus acidophilus surface layer protein A in colitis. The EMBO Journal (2015) 34, 881-895

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Vitamin D for Crohn’s Disease!

Researchers conducted a double-blind randomized placebo-controlled study, assigning 27 Crohn’s disease (CD) patients in remission to 2000 IU/day of vitamin D3 or placebo for 3 months. They determined intestinal permeability (IP), plasma-cathelicidin (LL-37), human-beta-defensin-2 (hBD2), disease activity [Crohn’s Disease Activity Index (CDAI)], c-reactive protein (CRP), fecal calprotectin, Quality of Life (QoL) and serum vitamin d (25(OH)D) at 0 and 3 months. Results showed that at 3 months, 25(OH)D concentrations were significantly higher in the treated group, and intra-group analysis showed increased LL-37 [an antimicrobial peptide (AMP) of the innate immune system expressed by the gastrointestinal epithelium] concentrations, and maintenance of IP measures. In contrast, in the placebo group, the small bowel and gastro-duodenal permeability increased from baseline. At 3 months, patients with 25(HO)D levels ≥ 75 nmol/L had significantly lower CRP, higher QoL, higher LL-37 concentrations and lower CDAI scores compared to those with lower 25(OH)D levels.

T Raftery, et al. Effects of vitamin D supplementation on intestinal permeability, cathelicidin and disease markers in Crohn’s disease: Results from a randomized double-blind placebo-controlled study. United Euro Gastro Journal 2015, Vol. 3(3) 294-302

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Vitamin D for gut microbiome and GI function?

Vitamin D is known for its effects on bone mineralization, inflammatory processes and immunomodulatory properties, which positively influences human health, but in-vivo data on its effects on human gut microbiome are missing. Researchers conducted an open-label, interventional pilot study to investigate the effects of oral vitamin D3 on the human mucosa-associated and stool microbiome as well as CD8+ T cells in healthy volunteers. Sixteen participants were endoscopically examined to access a total of 7 sites, and researchers sampled stomach, small bowel, colon, and stools before and after 8 weeks of vitamin D3 supplementation. Weeks 1-4 participants took a weekly dose representing 140 IU/Kg body weight per day up to a max of 68,600 IU/week (9,800 IU/day). The following 4 weeks they took half the amount (70 IU/Kg body weight per day up to 34,300 IU/week (4,900 IU/day). Supplementation changed the gut microbiome in the upper GI tract (gastric corpus, antrum and duodenum). Researchers found a decreased relative abundance of Gammaproteobacteria including Pseudomonas spp., Escherichia/Shigella spp. and increased bacterial richness. No major changes occurred in the terminal ileum, appendiceal orifice, ascending colon, and sigmoid colon or in stool, but the CD8+ T cell fraction was significantly increased in the terminal ileum. They concluded that vitamin D3 modulates the gut microbiome of the upper GI tract which might explain its positive influence on GI diseases such as inflammatory bowel disease or bacterial infections. Local effects demonstrate pronounce regional differences in the response of the GI microbiome to external factors.

M Bashir, et al. Effects of high doses of vitamin D3 on mucosa-associated gut microbiome vary between regions of the human gastrointestinal tract. Eur J Nutr. 2015 Jul 1. [Epub ahead of print]

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