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The Anti-Microbial Peptides
 Moderated by: Prof Trevor Marshall Page:  First Page Previous Page  1  2  3  4   
 

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TikBitten
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 Posted: Wed May 28th, 2008 18:07

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 Frans wrote:the problem then gets bigger and bigger as the bacterial load gets higher and higher, this will competitively displace 1,25D from the VDR, disabling it more and more, leading to lower AMPs etc.

the higher levels of 1,25D are there, but are just not high enough to get capnine, 25D and other antagonists out of the way and activate the VDR

the bacteria win the competition...

Hope this helps, Frans


 

If the scenario above, as presented by Frans, is correct what is the general consensus to the following thoughts:

Item 1
Isn't capnine (like 1,25D and 25D) a key marker of Th1 chronic inflammation?   And if so, is there a Quest or Labcorp test to check capnine tissue levels? 

Item 2
Could the "floaters" that appear so commonly in the eyes of Th1 patients actually be biofilm elements?  And if so, simple visual evidence of the condition?

Item 3
Is capnine the greater antagonistic culprit and, if so, does that shift the therapeutic level of 25,D of <= 12 ng/mL upwards?  And the degree, of course, of emphasis on dietary intake of VitD and sunlight avoidance?   

TikBitten




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Dx:Neurborreliosis 8/05|25D=46 1,25D=62 10/07|Avoid Sun&VitD since 10/07|Started Ph1&NoIRs 3/08|25D=18 3/08|25D=17 6/08|ModPh2 6/08|Ph2 9/08 stopped NoIRs|Ph3 1/09|25D=13 3/09|25D=10 5/09|25D=11 7/09|25D=15 9/09|25D=9 4/11
ChrisW
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 Posted: Fri May 30th, 2008 02:51

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Thanks for your feedback Frans, Wrotek & Trevor,

1.) After reading up on Interferon gamma and "Vitamin D Discovery outpaces FDA decision making" I’ve reached the conclusion that... the rise in 1,25D is the body’s response to infection.

As far as we know the microbiota are NOT directly attempting to stimulate 1,25D as this would reduce their chances of survival. Please correct me if I’m wrong.

2.) However, as 1,25D reaches very high concentrations it blocks other receptors thereby reducing production of other AMP’s.

Is there any evidence that 1,25D is of benefit to the invaders at the lower concentrations?

Thanks again,
Chris :)



____________________
CFS osteoporosis 125D60 25D16.4 Ph1Oct07 Ph2Dec07 calcium magnesium NoIRs, low lux home, limited outings, covered up.
Prof Trevor Marshall
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 Posted: Fri May 30th, 2008 04:26

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Chris said:
the rise in 1,25D is the body’s response to infection
Indeed. If you look at Figure 1 in "Vit D discovery..." you will see Interferon-gamma as input to the upregulation of transcription of CYP27B1. In a healthy individual this would upregulate 1,25-D; upregulate VDR transcription, and enhance innate immune response. The metagenome has evolved to thwart that action by blocking VDR.

That is the reason that I talk about "Th1" disease - Interferon-gamma is the common thread in all these symptomatic variations, and IFg implies Th1 (by definition).
 

Ute
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 Posted: Thu Jan 28th, 2010 00:29

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http://www.nature.com/nature/journal/v463/n7279/full/nature08698.html
Nature 463, 369-373 (21 January 2010) ...Accepted 24 November 2009
Thomas Becker1, et al..

An important class of immune effector molecules to fight pathogen infections are antimicrobial peptides (AMPs) that are produced in plants and animals1. In Drosophila, the induction of AMPs in response to infection is regulated through the activation of the evolutionarily conserved Toll and immune deficiency (IMD) pathways2. Here we show that AMP activation can be achieved independently of these immunoregulatory pathways by the transcription factor FOXO, a key regulator of stress resistance, metabolism and ageing. ….



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CFS/FM/IBS part.thyroidectomy osteopenia food sensit 125D71 25D10.8 Ph1Nov07 Ph2Jan08 Ph3May08 T3/T4 cal/mag Tri-Est Progest./ Milk thistle
Prof Trevor Marshall
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 Posted: Thu Jan 28th, 2010 07:32

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One needs to be very careful in using animal models to help us understand the human immune system. Even the immune system of other mammals, such as mice, is significantly different from that of man (mice have a different number and function of TLR receptors, for example).

Even in higher primates there are differences in the innate immune system, such as transcription of Cathelicidin - which appears unique to man. For example - ponder SIV and HIV :)

The reliance upon animal models is one of the reasons that Biology has failed to produce solutions in the past few decades. Now that understanding of Genomes and transcription has overtaken that disability, there is an explosion of knowledge in-silico :)
 

Ute
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 Posted: Thu Jan 28th, 2010 07:52

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Excuse me, please,

I was inattentive - yes, I knew that animal models don't count any more....



____________________
CFS/FM/IBS part.thyroidectomy osteopenia food sensit 125D71 25D10.8 Ph1Nov07 Ph2Jan08 Ph3May08 T3/T4 cal/mag Tri-Est Progest./ Milk thistle
Prof Trevor Marshall
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 Posted: Thu Jan 28th, 2010 08:54

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I didn't mean to be critical - my comment was just a reminder :)
 


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