Kickas.org Forums Treatments, Drugs and Alternatives NSD and diet-related; Immune regulation - TNF, A20, etc

Very promising research is going on in regards to how our body properly regulates its immune response.

In reply to:

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September 29, 2000
Investigating Inflammation

The body's immune system is a formidable force. Upon detecting invaders, it launches a no-holds barred attack--the inflammatory response. But once it has the assailants under control, the immune system must reign in the inflammation it caused because, if left unregulated, it can do extensive tissue damage. According to a report published today in the journal Science, researchers have determined that a little-known molecule called A20 plays a key role in quelling inflammation. And the discovery could lead to new treatment for inflammatory diseases such as rheumatoid arthritis and ulcerative colitis.

Thinking that A20 was only produced in a few tissues, researchers at the University of Chicago originally set out to pinpoint A20's function in certain white blood cells in the intestine. In order to do that, they created a line of genetically altered mice that lacked the A20 gene. But a few weeks after birth, these so-called "knockout mice" spontaneously developed serious inflammation and tissue damage in several organs (see photo). Exposing them to inflammation-triggering substances led to septic-shock. Normal mice, in contrast, exhibited no symptoms, even when given 10-fold higher doses of the substances. "We found that A20 was absolutely essential for down-regulating the inflammatory response and averting the damage unrestrained inflammation can cause in multiple tissues," says team member Averil Ma.

Specifically A20 appears to call off a substance known as tumor necrosis factor (TNF). Though critical to the immune response, prolonged release of TNF leads to severe injury. Although the FDA has approved antibodies to TNF for the purposes of treating inflammatory disorders, Ma notes that "these therapies are not always effective." But the discovery of A20's crucial regulatory role should open up new therapeutic avenues. "We can now hope to block cellular responses to TNF," Ma remarks, "in addition to trying to block TNF itself." --Kate Wong
http://www.sciam.com/article.cfm?articleID=0002DC72-8E6B-1C61-B882809EC588ED9F&pageNumber=1&catID=1

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"So long and thanks for all the fish" - Hitch Hikers Guide To The Galaxy

Here is the picture that goes with that article:



... I feel like the second mouse ...

"So long and thanks for all the fish" - Hitch Hikers Guide To The Galaxy

Oh good. Then that'll be yet another immuno-suppressant I don't intend to be taking.

Love-melancholy is twofold: the first is that affection of those which put God for their object, and are altogether about prayer, fasting, etc.; the other about women.

I wouldn't be too quick to call A20 an immuno-suppressant. Or at least perhaps avoid comparing it with traditional immune-suppressants. I suspect this may be a bit different. This time we are talking about using our bodies built in method for regulating its' immune response.

Imagine getting a bad stomach-flu with fevers, sweats, aches and pains all over.. And when your immune system killed off the pathogen - it forgot to reign in it's attack. You would be permanently fixed in this painful state. The article suggests that if your body is not producing "A20" then your immune system will degenerate into an unregulated perpetual flare. Doesn't this sound familiar?

"So long and thanks for all the fish" - Hitch Hikers Guide To The Galaxy

Erm ... OK then ... would 'anti-inflammatory', or possibly 'immune-modulating' be better?

Love-melancholy is twofold: the first is that affection of those which put God for their object, and are altogether about prayer, fasting, etc.; the other about women.

The mice missing A20 molecule were extremely sensitive to certain "inflammation-triggering substances" (antigens). Whilst the normal mice were fine, even at 10-fold higher doses.

"inflammation-triggering substances" means foreign proteins.. whether they be Klebsiella antigens, peanut antigens, whatever. Now think about what happens when some AS'ers eat cashew's or wheat-gluten ... I would consider this shows another parallel between AS and the research done in Chicago.

"So long and thanks for all the fish" - Hitch Hikers Guide To The Galaxy

Who knows .. I have often wondered when I see new research that scientists / people are a bit quick to place a drug into the most hyped up category available. Whether it be "anti-TNF" or "Cox-2 inhibitor".

What I am trying to say (clumsily) is that.. well... if I took a blood test before and after a week of good exercise or NSD - and found that my TNF and Cox-2 levels had dropped. Would I then call exercise a "Cox-2 inhibitor". Or would I call NSD an "anti-TNF" immune suppressor ?

The question to me is.. does this "A20" chemical work like other "Anti-TNF" drugs. And I suspect that it does not.


"So long and thanks for all the fish" - Hitch Hikers Guide To The Galaxy

I'm no scientist bilko, you were probably right the first time ! hehee

"So long and thanks for all the fish" - Hitch Hikers Guide To The Galaxy

Indeed. This research is stupid as it answers the question:

"How can WE influence off the inflammatory response."

but the question should be

"Why does the body fires this inflammatory response."

Our immune systems are fine, we have something triggering a normal response.
if the response is severe, then the cause must be severe.
They cure is to find this 'something', the first lead is the food as our food-changes (diet) ease off the immune reaction without interfering with the immune system processes.

typical modern-western research: high-tech answers to stupid questions.

Arjan

Hi Zark,
There was a time, pretty long ago, that I considered myself a beginning scientist, at least I did research in related fields. That does not mean that my opinon is more worthwile than any of the others , just my two cents worth.
The question to be answered is: does this inflammation downscaling molecule play a role in the sequence that trigger our illness. If we consider AS as a genetically determined wrong reaction of the immune system to a normal gut flora and we see the HlaB27or related factor that is confused for some intestinal bacteria (or part of bacteria) as the cause of this wrong reaction. In that case this new A20 will do nothing good. It is even further off from the origin of the disease then the TNF-blockers that are used pretty successfully nowadays in suppressing the AS symptoms.
Best regards,
Gerard

"Walk gently, breathe peacefully, laugh hysterically." -Nelson Mandela-