Kickas.org Forums Ankylosing Spondylitis General Discussion #1 AS Web Support Group Immune responce vs diet

One thing I am confused about. Maybe there is not an answer. If the possible cause of AS is through diet and genetics then how does the immune system response factor in?

2 days before I come down with the flu or cold I develop a flare. One month before I notices an absessed tooth my arm was flaring from the back of my neck to my wrist. After taking care of the problem the flare is starting to subside. I have not read about any tie-in between the immune response I normally get and the root cause of AS. Assuming diet does work what re-codes my immune system to stop attacking my body every time I get sick?

Does anyone have any info on this?

Thanks,

Tim

Thats a very interesting question Tim I cant answer but would be interested to know the answer.
Kevin

Using molecular mimicry theory the answer would be

1) genetics- because the hla-b27 gene has similar structure to the collagen in the joints it means that when the immune system is exposed to klebsiella there can be an auto-immune response i.e. attacking klebsiella + collagen. without hla-b27 (or similar gene) there is no reason for the immune system to become confused.

2) immune system - because the immune system is involved in the disease process then anything that affects the immune system - colds, flu etc can have an effect on the disease.

3) diet - diet can increase or decrease the amount of klebsiella in the digestive tract making the auto-immune reaction stronger or weaker. diet can also influence intestinal permeability which affects how much of the bacteria in the gut the immune system can "see".

hope that helps

After being tested 5 times I am HLA-B27 negative. I can track your statement forward into the process but I am confused how it would reverse itself. Once the process has started how does the reduction of Klebsiella reduce the immune response?

Hi, Tim:

In molecular mimicry, it is the secondary immune system that participates in the lock-and-key misidentification of the Osp (Outer surface protein).

There is some tendency for AS symptoms to calm down when getting a cold, but exacerbate somewhat when getting the flu, depending upon what was going on before. There are several reasons for this--one is that 'anergy' depletes the immune components and another might be related to the indiscriminate increased production of all immune agents during illness.

The only thing diet accomplishes is some "substrate modulation," (growth medium change) to reduce which bacteria are encouraged to grow over others, but even if diet is working fine one day, if something happens to open up new lesions in the intestinal tract, more AS activity will happen the next day because there is more bacteria made available to the lymph nodes. This causes greater production of the immunoglobulin specific to Klebsiella--IgA-Kp.

We develop a "library" of bad actors (various pathogens), and the majority of these are stored in our intestinal tract, so that is why it is said that 80% of our immune system is in our guts--it is the helper cells that constantly circulate through the lymph (AS is a disease of lymph) looking for new invasions of familiar amino acid sequences (the Klebsiella sequence is the hexamer QTDRED). The thing that reprograms our immune system is more Klebsiella crossing the epithelium (thin barrier covering gut) into the blood and lymph. Our defenses are already heightened to this germ from previous waves of invasion, so the whistle blows and factory churns out more IgA-Kp.

I described the immune system as a sort of Rube Goldberg contraption--but it seems that way--too many things going on in too subtle ways down layer upon layer to infinitesimal levels dealing with single molecules.

Well, that's how I see it, anyway,

HEALTH,
John

So Jroc, are you suggesting that perhaps there may be a difference in the severity of the disease being hla positive vs negative? Thx for the post, I found it very interesting?

Good questions Tim!!

Great question and great response from John. That explains to me how, long before I developed my first flare up of uveitis, every time I would get sick with a virus, I'd have horrible joint pain. Every possible joint would hurt so badly, even if I just had a "cold." I never knew why, and one time a friend who was studying nursing looked at me when I was dealing with a cold and complaining of my joints, and she said, "that is NOT normal." Always learning!
Thanks again,
Jan

I'm not suggesting anything, just trying to explain the little bit about Prof Ebringers theory that I have read. If an hla-b27 negative with AS has one of the similar genes (B39/40, B7, or H8) then the gene could have a less similar surface protein to klebeislla than B27. it could even work the other way and be more similar than B27. I'm not sure how this affects the severity as there are numerous other factors but I can see how the more similar the gene and germ are then the more likely chance of an auto-immune response. Just guessing though.

Thanks everyone for your replies. Is there any research planed in the future to check the molecular mimicry with other genes found other than HLA-B27?

Hi, Tim:

Yes, Ebringer is going to check on HLA B51 (Behcet's Disease) for mimicry to Klebsiella pneumoniae, but it is best to understand that despite the HLA B27 negative result, if you have AS it is the same mechanism. Ebringer never wanted to complicate his results by including B27- people in the studies and it was his general opinion after observing this group in his clinic for 20 years, that their AS disease process was not typical and seemed to be less destructive, overall. At that time he did not commit to whether diet worked for the neg group because he had not included them in his scientific diet studies, however, he was of the strong opinion that diet should be part of their therapy, too, and encouraged them to follow his LSD.

Since that time, I have communicated with many B27- AS+ individuals and the greater majority do respond to diet and some (when tried/necessary) to antibiotics.

The tissue typing MHC system is not really a full picture and there is a lot of 'blur' or overlapping characteristics.

AS is the exception to the "Whatever does not kill us makes us stronger" adage, and we should be able to predict new diseases when the more pathogenic protein sequences become identified by our bodies. We now harbor over 200 different bacteria and 3000+ viruses but the possibilities are endless, so every time we encounter a new pathogen it is a new opportunity for not only acute disease, but also a chronic, lingering malaise.

KickAS,
John