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home:pathogenesis:vitamind:metabolism [01.01.2019]
sallieq [Metabolism of vitamin D and the Vitamin D Receptor]
home:pathogenesis:vitamind:metabolism [01.01.2019]
sallieq [Notes and comments]
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 Located in the nucleus of a variety of cells including immune cells, the VDR is a control system of sorts. When exposed to infection and damage, especially that which is caused by pathogens, the body begins to convert the inactive form 25-D into the active form, 1,25-D. As cellular concentrations of 1,25-D increase, 1,25-D activates the VDR, turning on any number of genes the receptor transcribes.  Located in the nucleus of a variety of cells including immune cells, the VDR is a control system of sorts. When exposed to infection and damage, especially that which is caused by pathogens, the body begins to convert the inactive form 25-D into the active form, 1,25-D. As cellular concentrations of 1,25-D increase, 1,25-D activates the VDR, turning on any number of genes the receptor transcribes. 
- [[https://autoimmunityresearch.org/hormones.pdf|Hormonal changes result from change in 1,25 dihydroxyvitamin-D]]+  
 +[[https://autoimmunityresearch.org/hormones.pdf|Hormonal changes result from change in 1,25 dihydroxyvitamin-D]]
  
 According to a 2010 analysis, the VDR significantly affects 229 human genes. Many of these genes have long been associated with autoimmune diseases and cancers including, for example, the genes IRF8 (linked to multiple sclerosis), and PTPN2 (connected to Crohn's disease and type I diabetes).(({{pubmed>long:20736230}})) The activation of certain genes also leads to the synthesis of antimicrobial peptides. The antimicrobial peptides are the body's "natural antibiotics" and have a potent anti-bacterial effect. According to a 2010 analysis, the VDR significantly affects 229 human genes. Many of these genes have long been associated with autoimmune diseases and cancers including, for example, the genes IRF8 (linked to multiple sclerosis), and PTPN2 (connected to Crohn's disease and type I diabetes).(({{pubmed>long:20736230}})) The activation of certain genes also leads to the synthesis of antimicrobial peptides. The antimicrobial peptides are the body's "natural antibiotics" and have a potent anti-bacterial effect.
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 <blockquote> <blockquote>
-Not sure where this should go. Here? Psoriasis? Innate immunity?+Not sure where this should go. Here? Psoriasis? Innate immunity?  MOVED >Psoriasis
  
 PLoS One. 2009 Jul 22;4(7):e6340. PLoS One. 2009 Jul 22;4(7):e6340.
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 Peric M, Koglin S, Dombrowski Y, Gross K, Bradac E, Büchau A, Steinmeyer A, Zügel U, Ruzicka T, Schauber J. Peric M, Koglin S, Dombrowski Y, Gross K, Bradac E, Büchau A, Steinmeyer A, Zügel U, Ruzicka T, Schauber J.
-Department of Dermatology and Allergology, Ludwig-Maximilians-University, Munich, Germany. 
-Abstract 
-Antimicrobial peptides (AMPs) are strongly expressed in lesional skin in psoriasis and play an important role as proinflammatory "alarmins" in this chronic skin disease. Vitamin D analogs like calcipotriol have antipsoriatic effects and might mediate this effect by changing AMP expression. In this study, keratinocytes in lesional psoriatic plaques showed decreased expression of the AMPs beta-defensin (HBD) 2 and HBD3 after topical treatment with calcipotriol. At the same time, calcipotriol normalized the proinflammatory cytokine milieu and decreased interleukin (IL)-17A, IL-17F and IL-8 transcript abundance in lesional psoriatic skin. In contrast, cathelicidin antimicrobial peptide expression was increased by calcipotriol while psoriasin expression remained unchanged. In cultured human epidermal keratinocytes the effect of different vitamin D analogs on the expression of AMPs was further analyzed. All vitamin D analogs tested blocked IL-17A induced HBD2 expression by increasing IkappaB-alpha protein and inhibition of NF-kappaB signaling. At the same time vitamin D analogs induced cathelicidin through activation of the vitamin D receptor and MEK/ERK signaling. These studies suggest that vitamin D analogs differentially alter AMP expression in lesional psoriatic skin and cultured keratinocytes. Balancing AMP "alarmin" expression might be a novel goal in treatment of chronic inflammatory skin diseases. 
  
 PMID: 19623255 PMID: 19623255
home/pathogenesis/vitamind/metabolism.txt · Last modified: 01.01.2019 by sallieq
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