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Helicobacter pylori infection protection by the body’s increasing Vitamin D receptors – Nov 2013

Helicobacter pylori Induces Increased Expression of the Vitamin D Receptor in Immune Responses.

Helicobacter. 2013 Nov 4. doi: 10.1111/hel.12102.
Guo L, Chen W, Zhu H, Chen Y, Wan X, Yang N, Xu S, Yu C, Chen L.
Department of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China; Department of Gastroenterology, The Affiliated Hospital, College of Medicine, Ningbo University, Ningbo, 315020, China.

BACKGROUND: Vitamin D receptor (VDR) is a member of the nuclear receptor family of transcription factors that play a critical role in innate immunity. This study examined the role of VDR in gastric innate immune defence against the gastric pathogen Helicobacter pylori.

MATERIALS AND METHODS: Seventeen H. pylori-infected patients and sixteen controls participated in the study. The GES-1 cells were transfected with siRNA or incubated with or without 1α,25(OH)2 D3 (100 nmol/L) then infected with H. pylori. VDR, cathelicidin antimicrobial protein (CAMP), and cytokine mRNA expression levels in normal and H. pylori-infected gastric mucosa and GES-1 cells was determined by qRT-PCR and correlated with the histopathologic degree of gastritis. Bactericidal activity was measured by using a colony-forming unit assay.

RESULTS: Vitamin D receptor mRNA expression levels were significantly upregulated in H. pylori-infected patients and positively correlated with chronic inflammation scores. There was a significant positive correlation between VDR and CAMP mRNA expression in H. pylori-positive gastric mucosa. VDR siRNA reduced H. pylori-induced CAMP production and conversely increased IL-6 and IL8/CXCL8 expression levels. The vitamin D agonist 1α,25(OH)2 D3 increased CAMP expression and reduced cytokine activation in GES-1 cells infected with H. pylori. 1α,25(OH)2 D3 could enhance the intracellular killing of the replicating bacteria, but the presence of siVDR and siCAMP led to a decline in its bactericidal ability.

CONCLUSIONS: The expression of VDR and CAMP in the gastric epithelium is up-regulated in the case of H. pylori infection; thus, VDR plays an important role in gastric mucosa homeostasis and host protection from H. pylori infection.

PMID: 24188043

See also VitaminDWiki

Vitamin D Receptor category has the following

410 studies in Vitamin D Receptor category

Vitamin D tests cannot detect Vitamin D Receptor (VDR) problems
A poor VDR restricts Vitamin D from getting in the cells
It appears that 30% of the population have a poor VDR (40% of the Obese )

A poor VDR increases the risk of 55 health problems  click here for details
The risk of 44 diseases at least double with poor Vitamin D Receptor as of Oct 2019

VDR at-home test $29 - results not easily understood in 2016
There are hints that you may have inherited a poor VDR

Compensate for poor VDR by increasing one or more:

1) Vitamin D supplement
  Sun, Ultraviolet -B
Vitamin D in the blood
and thus in the cells
2) MagnesiumVitamin D in the blood
 AND in the cells
3) Omega-3 Vitamin D in the cells
4) Resveratrol Vitamin D Receptor
5) Intense exercise Vitamin D Receptor
6) Get prescription for VDR activator
   paricalcitol, maxacalcitol?
Vitamin D Receptor
7) Quercetin (flavonoid) Vitamin D Receptor
8) Zinc is in the VDRVitamin D Receptor
9) BoronVitamin D Receptor ?,
10) Essential oils e.g. ginger, curcuminVitamin D Receptor
11) ProgesteroneVitamin D Receptor
12) Infrequent high concentration Vitamin D
Increases the concentration gradient
Vitamin D in the cells
13) Sulfroaphane and perhaps sulfurVitamin D Receptor

Note: If you are not feeling enough benefit from Vitamin D, you might try increasing VDR activation. You might feel the benefit within days of adding one or more of the above

Far healthier and stronger at age 72 due to supplements Includes 6 supplements that help the VDR

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3619 Helicobacter pylori.pdf PDF 2014 admin 16 Feb, 2014 03:19 427.49 Kb 661
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