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The dietary histone deacetylase inhibitor sulforaphane induces human beta-defensin-2 in intestinal epithelial cells.
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The dietary histone deacetylase inhibitor sulforaphane induces human beta-defensin-2 in intestinal epithelial cells.
Full Study: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2561129/?tool=pubmed
Immunology. 2008 Oct;125(2):241-51.
The dietary histone deacetylase inhibitor sulforaphane induces human beta-defensin-2 in intestinal epithelial cells.
Schwab M, Reynders V, Loitsch S, Steinhilber D, Schröder O, Stein J.
First Department of Medicine-ZAFES, Johann Wolfgang Goethe-University Frankfurt, Germany. m.schwab@med.uni-frankfurt.de
Antimicrobial peptides like human beta-defensin-2 (HBD-2) play an important role in the innate immune system protecting the intestinal mucosa against bacterial invasion. The dietary histone deacetylase (HDAC) inhibitors sulforaphane (SFN) and butyrate have received a great deal of attention because of their ability to simultaneously modulate multiple cellular targets involved in cellular protection. In this study the influence of SFN and butyrate on HBD-2 expression as well as the molecular pathways involved in SFN-mediated induction of HBD-2 were scrutinized. Treatment of Caco-2, HT-29 and SW480 cells with SFN led to a time- and dose-dependent upregulation of HBD-2 mRNA expression as determined by semi-quantitative reverse transcription-polymerase chain reaction. Moreover, HBD-2 protein production increased in response to SFN, measured by enzyme-linked immunosorbent assay. Induction of HBD-2 was also observed in response to butyrate. Immunofluorescence analysis revealed that the protein was localized in the cytosol. Coincubation of SFN with a vitamin D receptor (VDR), or an extracellular-regulated kinase 1/2 or a nuclear factor-kappaB inhibitor all reduced HBD-2 mRNA upregulation. In contrast, transfection of cells with a dominant-negative peroxisome proliferator-activated receptor gamma (PPARgamma) mutant vector to inhibit PPARgamma wild-type action and inhibition of p38 mitogen-activated protein kinase (MAPK) signalling did not affect SFN-mediated upregulation of HBD-2 mRNA. Moreover, SFN induced the expression of VDR, PPARgamma and phosphorylated ERK1/2 but did not affect p38 MAPK activation. The data clearly demonstrate for the first time that the dietary HDAC inhibitor SFN is able to induce antimicrobial peptides in colonocytes. In this process HBD-2 expression is regulated via VDR, mitogen-activated protein kinase kinase/extracellular-regulated kinase and nuclear factor-kappaB signalling.
Immunology. 2008 Oct;125(2):241-51.
The dietary histone deacetylase inhibitor sulforaphane induces human beta-defensin-2 in intestinal epithelial cells.
Schwab M, Reynders V, Loitsch S, Steinhilber D, Schröder O, Stein J.
First Department of Medicine-ZAFES, Johann Wolfgang Goethe-University Frankfurt, Germany. m.schwab@med.uni-frankfurt.de
Antimicrobial peptides like human beta-defensin-2 (HBD-2) play an important role in the innate immune system protecting the intestinal mucosa against bacterial invasion. The dietary histone deacetylase (HDAC) inhibitors sulforaphane (SFN) and butyrate have received a great deal of attention because of their ability to simultaneously modulate multiple cellular targets involved in cellular protection. In this study the influence of SFN and butyrate on HBD-2 expression as well as the molecular pathways involved in SFN-mediated induction of HBD-2 were scrutinized. Treatment of Caco-2, HT-29 and SW480 cells with SFN led to a time- and dose-dependent upregulation of HBD-2 mRNA expression as determined by semi-quantitative reverse transcription-polymerase chain reaction. Moreover, HBD-2 protein production increased in response to SFN, measured by enzyme-linked immunosorbent assay. Induction of HBD-2 was also observed in response to butyrate. Immunofluorescence analysis revealed that the protein was localized in the cytosol. Coincubation of SFN with a vitamin D receptor (VDR), or an extracellular-regulated kinase 1/2 or a nuclear factor-kappaB inhibitor all reduced HBD-2 mRNA upregulation. In contrast, transfection of cells with a dominant-negative peroxisome proliferator-activated receptor gamma (PPARgamma) mutant vector to inhibit PPARgamma wild-type action and inhibition of p38 mitogen-activated protein kinase (MAPK) signalling did not affect SFN-mediated upregulation of HBD-2 mRNA. Moreover, SFN induced the expression of VDR, PPARgamma and phosphorylated ERK1/2 but did not affect p38 MAPK activation. The data clearly demonstrate for the first time that the dietary HDAC inhibitor SFN is able to induce antimicrobial peptides in colonocytes. In this process HBD-2 expression is regulated via VDR, mitogen-activated protein kinase kinase/extracellular-regulated kinase and nuclear factor-kappaB signalling.
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Re: The dietary histone deacetylase inhibitor sulforaphane induces human beta-defensin-2 in intestinal epithelial cells.
Sulforaphane along with Vitamin D, effective help produce antimicrobial peptides, and enhance the regulation of beta-defensins.
When there is sufficient 1,25-dihydroxyvitamin D3, the immune system can produce cathelicidins, which are antimicrobial peptides. This can provide defense against bacteria, fungi and parasites. Another defense is the alpha- and beta-defensins. This is also a factor in acne as well.
That said, sulforaphane can induce beta-defensins and vitamin D can provide antimicrobial peptides.
It's possible that each of the above operate as co-factors to protect the skin barrier, as well as the intestinal lining, allowing proper defense of skin & hair via stem cell health and its innate immunity.
The LGR5 gene, which is linked to hair growth in mice is likely affected by this mechanism. This is to say that stem cells can be preserved in male pattern baldness and protection against various assaults.
Since I've optimized my vitamin D and taken Sulforaphane (9 mgs) per day, MPB seems like a thing of the past.
When there is sufficient 1,25-dihydroxyvitamin D3, the immune system can produce cathelicidins, which are antimicrobial peptides. This can provide defense against bacteria, fungi and parasites. Another defense is the alpha- and beta-defensins. This is also a factor in acne as well.
That said, sulforaphane can induce beta-defensins and vitamin D can provide antimicrobial peptides.
It's possible that each of the above operate as co-factors to protect the skin barrier, as well as the intestinal lining, allowing proper defense of skin & hair via stem cell health and its innate immunity.
The LGR5 gene, which is linked to hair growth in mice is likely affected by this mechanism. This is to say that stem cells can be preserved in male pattern baldness and protection against various assaults.
Since I've optimized my vitamin D and taken Sulforaphane (9 mgs) per day, MPB seems like a thing of the past.
_________________
My regimen
http://www.immortalhair.org/mpb-regimen
Now available for consultation (hair and/or health)
http://www.immortalhair.org/health-consultation
Re: The dietary histone deacetylase inhibitor sulforaphane induces human beta-defensin-2 in intestinal epithelial cells.
Great info.
From this evidence, I'm thinking that Sulforaphane could be used or at least considered as a therapeutic agent in treating intestinal dysbiosis; due to its antimicrobial and possible intestinal barrier improving functions (along with Vit. D), like CS said.
Vitamind D has been previously suggested as beneficial for treating and preventing Crohn's disease: http://www.nleducation.co.uk/resources/abstracts/vitamin-d-vs-crohns-ibd-cancer
Quoting:
Given the multitude of benefits of both Vit. D and Sulphoraphane on health, including AGA, and the relatively low cost of them, it would seem almost crazy (or illogical if you wish) not to consider them, at least.
From this evidence, I'm thinking that Sulforaphane could be used or at least considered as a therapeutic agent in treating intestinal dysbiosis; due to its antimicrobial and possible intestinal barrier improving functions (along with Vit. D), like CS said.
Vitamind D has been previously suggested as beneficial for treating and preventing Crohn's disease: http://www.nleducation.co.uk/resources/abstracts/vitamin-d-vs-crohns-ibd-cancer
Quoting:
This study revealed that Vitamin D acts directly on 2 key genes related to Croh’s called the beta defensin 2 gene, which encodes an antimicrobial peptide, and the NOD2 gene that alerts cells to the presence of invading microbes. If NOD2 is deficient or defective, it cannot combat invaders in the intestinal tract.
Given the multitude of benefits of both Vit. D and Sulphoraphane on health, including AGA, and the relatively low cost of them, it would seem almost crazy (or illogical if you wish) not to consider them, at least.
LittleFighter- Posts : 1114
Join date : 2009-07-07
Re: The dietary histone deacetylase inhibitor sulforaphane induces human beta-defensin-2 in intestinal epithelial cells.
My mother faithfully takes 30 mg sulforophane daily, she is very pleased with it.
Amaranthaceae- Posts : 1368
Join date : 2008-07-15
Location : Copenhagen
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