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Autoimmune Diseases Caused by Bacteria?

Daffodil

Senior Member
Messages
5,875
Hi All. I am wondering what everyone thought about the theory that all autoimmune diseases are caused by intracellular bacterial infections.

The more research I do, the more evidence I find that this could be the case. I keep coming across patient stories of recovery or improvement from RA, MS, Lupus, Sarcoidosis, etc....even Scleroderma... with long-term antibiotics.

Thanks
 

Jonathan Edwards

"Gibberish"
Messages
5,256
Hi All. I am wondering what everyone thought about the theory that all autoimmune diseases are caused by intracellular bacterial infections.

The more research I do, the more evidence I find that this could be the case. I keep coming across patient stories of recovery or improvement from RA, MS, Lupus, Sarcoidosis, etc....even Scleroderma... with long-term antibiotics.

Thanks

Yes but we have about a century of experience of people with these diseases not getting better with antibiotics. And most rheumatologists can remember patients who had long term antibiotics for all sorts of reasons with no effect on their disease. And nobody has found an intracellular organism associated with these diseases to my knowledge.

Intracellular organisms do produce autoinflammatory disease with great regularity - particularly Reiter's disease, but as one would expect for an intracellular organism that is a T cell mediated disease, not an antibody related disease.

As far as I know there has never really been any evidence for infection causing autoimmunity. The idea arose as from a historical quirk - that when penicillin came out all the infectious disease physicians were out of a job, so became immunologists.
 

xrunner

Senior Member
Messages
843
Location
Surrey
Hi Jonathan,
There's truth in what you say about antibiotics but what would you say to Dr Wheldon who treated his wife MS and probably saved her life with an antibiotic protocol. From the little I read, mostly on forums, it doesn't work for everybody but for some people abx seem to help.
Perhaps here also we're dealing with different underlying diseases.

PS: I myself recovered from being housebound to having a decent life (no more pain, pem and insomnia) thanks to three years (on and off) multiple antibiotics when most consultants strongly advised against that and one even said to me I was totally mad in taking antibiotics.
 

Daffodil

Senior Member
Messages
5,875
Yes but we have about a century of experience of people with these diseases not getting better with antibiotics. And most rheumatologists can remember patients who had long term antibiotics for all sorts of reasons with no effect on their disease. And nobody has found an intracellular organism associated with these diseases to my knowledge.

Intracellular organisms do produce autoinflammatory disease with great regularity - particularly Reiter's disease, but as one would expect for an intracellular organism that is a T cell mediated disease, not an antibody related disease.

As far as I know there has never really been any evidence for infection causing autoimmunity. The idea arose as from a historical quirk - that when penicillin came out all the infectious disease physicians were out of a job, so became immunologists.
Hi Jonathan. I think they have found some kind of bacterial signaling in Sarcoidosis but you are right, no one can find the bacteria. It is well documented that antibiotics will cause remission in that disease, though.

I was not aware that there were many autoimmune patients who tried antibiotics long term and did not get any benefit.

Do all cases of Retier's have bacteria as a cause? I have a good friend who has had that for decades but his rheumatologists say he is not a candidate for antibiotics. I have read about C.Pn. being a trigger for Reiter's and indeed, he developed it after an unprotected sexual encounter.

sorry, my brain is severe mush today and I do not know what this means:
"...as one would expect for an intracellular organism that is a T cell mediated disease, not an antibody related disease."

Thanks
 
Last edited:

Daffodil

Senior Member
Messages
5,875
Maybe, since our immune system has shifted to Th1 to Th2, intracellular bacterial infections have gone unchecked and have spread, which might explain some patients' success with antibiotics.

I wonder if it is possible to find any story of someone actually going OFF antibiotics and still maintaining improvement.
 
Last edited:

Jonathan Edwards

"Gibberish"
Messages
5,256
Hi Jonathan,
There's truth in what you say about antibiotics but what would you say to Dr Wheldon who treated his wife MS and probably saved her life with an antibiotic protocol. From the little I read, mostly on forums, it doesn't work for everybody but for some people abx seem to help.
Perhaps here also we're dealing with different underlying diseases.

The trouble with MS is that you cannot draw any conclusions from treatment unless you do proper trials. The natural history of each episode is to improve so if you take any treatment when you are bad you are very likely to get better. Even in big trials there will be an effect called 'regression to the mean' (which is actually not a very good description). It is one of the many things that gets lumped into the 'placebo response'.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
Maybe, since our immune system has shifted to Th1 to Th2, intracellular bacterial infections have gone unchecked and have spread, which might explain some patients' success with antibiotics.

I wonder if it is possible to find any story of someone actually going OFF antibiotics and still maintaining improvement.

I never found, throughout my career, any evidence that the TH1/TH2 idea had anything to do with autoimmunity - just mice. And the people in autoimmunity who used to preach Th1 or Th2 now preach Th17 or Treg. It is all a lot of Greek myths to my mind. Just as there is a lot of dross in psychiatry I fear there is a lot of dross in immunology!
 

Jonathan Edwards

"Gibberish"
Messages
5,256
Hi Jonathan. I think they have found some kind of bacterial signaling in Sarcoidosis but you are right, no one can find the bacteria. It is well documented that antibiotics will cause remission in that disease, though.

I was not aware that there were many autoimmune patients who tried antibiotics long term and did not get any benefit.

Do all cases of Retier's have bacteria as a cause? I have a good friend who has had that for decades but his rheumatologists say he is not a candidate for antibiotics. I have read about C.Pn. being a trigger for Reiter's and indeed, he developed it after an unprotected sexual encounter.

sorry, my brain is severe mush today and I do not know what this means:
"...as one would expect for an intracellular organism that is a T cell mediated disease, not an antibody related disease."

Thanks

As far as I know antibiotics are no use for sarcoidosis. I did some studies in sarcoidosis myself on bacterial DNA and we found some strange things but they were non-specific and it looks as if a signal from human DNA looks a bit like bacterial DNA in this situation for some reason. I doubt there are any bacteria there.

Reiter's is by definition caused by an intracellular bacterium or something close to bacterium like chlamydia. The diagnosis presumes that causation. But antibiotics are of no value after the initial infection is cleared - which is usually no more than three weeks. The disease persists in the absence of any infection.

We would expect a disease caused by an intracellular organism to be T cell mediated because intracellular organisms are dealt with by CD8 T cells rather than antibodies, which do not get in to cells very well.
 

Daffodil

Senior Member
Messages
5,875
As far as I know antibiotics are no use for sarcoidosis. I did some studies in sarcoidosis myself on bacterial DNA and we found some strange things but they were non-specific and it looks as if a signal from human DNA looks a bit like bacterial DNA in this situation for some reason. I doubt there are any bacteria there.

Reiter's is by definition caused by an intracellular bacterium or something close to bacterium like chlamydia. The diagnosis presumes that causation. But antibiotics are of no value after the initial infection is cleared - which is usually no more than three weeks. The disease persists in the absence of any infection.

We would expect a disease caused by an intracellular organism to be T cell mediated because intracellular organisms are dealt with by CD8 T cells rather than antibodies, which do not get in to cells very well.
Thanks Jonathan. So..is CFS T cell mediated?

They say autoimmune diseases that are IgA mediated are "gut mediated". Does this mean that curing leaky gut (if possible) will cure the symdrome?

Or maybe the leaky gut is just a downstream effect..


Thanks
 

Art Vandelay

Senior Member
Messages
470
Location
Australia
Hi All. I am wondering what everyone thought about the theory that all autoimmune diseases are caused by intracellular bacterial infections.

The more research I do, the more evidence I find that this could be the case. I keep coming across patient stories of recovery or improvement from RA, MS, Lupus, Sarcoidosis, etc....even Scleroderma... with long-term antibiotics.

Here's a link to an Australian science show about chlamydia pneumonia being a possible cause of MS: http://www.abc.net.au/catalyst/stories/3572695.htm

The Marshall Protocol people definitely argue that intracellular bacterial can be responsible for many auto-immune diseases including sarcoidosis: http://mpkb.org/home/diseases

I've long suspected that my CFS/ME is caused by bacterial infection and I have improved significantly (and continue to improve) with antibiotics.
 

Daffodil

Senior Member
Messages
5,875
Here's a link to an Australian science show about chlamydia pneumonia being a possible cause of MS: http://www.abc.net.au/catalyst/stories/3572695.htm

The Marshall Protocol people definitely argue that intracellular bacterial can be responsible for many auto-immune diseases including sarcoidosis: http://mpkb.org/home/diseases

I've long suspected that my CFS/ME is caused by bacterial infection and I have improved significantly (and continue to improve) with antibiotics.
Hi Art. hee hee that name always makes me giggle.

I saw that abc.net video earlier today. so interesting. on cpnhelp.org I ran into some people who say that they not only cured their MS with antibiotics, but that they have been off them for years. I did not expect that.

I also read stories from people who did not respond to antibiotics.

I am glad they are helping you. If I had to guess, at this point, I would still stay the EBV triggered some disease process in me, which caused bacteria to spread....but the bacterial spreading is what is giving most of the symptoms. ...not even sure if that makes any sense.
 

Art Vandelay

Senior Member
Messages
470
Location
Australia
Hi Art. hee hee that name always makes me giggle.

Glad it makes you laugh!! :)

I saw that abc.net video earlier today. so interesting. on cpnhelp.org I ran into some people who say that they not only cured their MS with antibiotics, but that they have been off them for years. I did not expect that.

I've also read stories who have recovered from sarcoidosis, RA and Lyme for example after treatment with the MP too.

I am glad they are helping you. If I had to guess, at this point, I would still stay the EBV triggered some disease process in me, which caused bacteria to spread....but the bacterial spreading is what is giving most of the symptoms. ...not even sure if that makes any sense.

This makes perfect sense because it tallies with my experience. I am pretty sure I had some form of the bacteria in my system prior to getting EBV since I had a few symptoms already. My theory is that the EBV perhaps weakened my immune system so that the bacteria could spread? Or perhaps the broad spectrum antibiotics I was given first in error (I was originally mis-diagnosed with tonsillitis instead of EBV) cased the bacteria to mutate into cell-wall deficient forms and/or form biofilms.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
Thanks Jonathan. So..is CFS T cell mediated?

They say autoimmune diseases that are IgA mediated are "gut mediated". Does this mean that curing leaky gut (if possible) will cure the symdrome?

Or maybe the leaky gut is just a downstream effect..


Thanks

My thoughts about CFS are on the thread 'Do MEs cause CFS?' I suspect there is a T cell mediated type of ME but it may be a tiny minority. Mostly, we have no idea, I think.

I am not sure where the idea of IgA mediated autoimmune disease comes from but I doubt it has anything necessarily to do with gut. I am afraid there is a whole heap of nonsense out there about autoimmunity - even in the most high profile science journals. I do not know of any evidence for leakiness in the gut causing autoimmunity. As far as I am aware autoimmunity is caused mostly be genetics and by chance errors in B cell regulation - not much to do with the environment at all. In coeliac an environmental factor is involved but I doubt that has anything to do with leakiness.
 

Daffodil

Senior Member
Messages
5,875
My thoughts about CFS are on the thread 'Do MEs cause CFS?' I suspect there is a T cell mediated type of ME but it may be a tiny minority. Mostly, we have no idea, I think.

I am not sure where the idea of IgA mediated autoimmune disease comes from but I doubt it has anything necessarily to do with gut. I am afraid there is a whole heap of nonsense out there about autoimmunity - even in the most high profile science journals. I do not know of any evidence for leakiness in the gut causing autoimmunity. As far as I am aware autoimmunity is caused mostly be genetics and by chance errors in B cell regulation - not much to do with the environment at all. In coeliac an environmental factor is involved but I doubt that has anything to do with leakiness.
Hi Jonathan. That's exactly what I used to think, but then Rocephin resulted in HUGE dramatic improvements in my neurological symptoms, neck pain, lymph node swelling and aches. One researcher commented that they believe that the Rocephin is so powerful and broad spectrum, it was acting on translocated bacteria from the gut.

Thanks:)
 

Daffodil

Senior Member
Messages
5,875
Glad it makes you laugh!! :)



I've also read stories who have recovered from sarcoidosis, RA and Lyme for example after treatment with the MP too.



This makes perfect sense because it tallies with my experience. I am pretty sure I had some form of the bacteria in my system prior to getting EBV since I had a few symptoms already. My theory is that the EBV perhaps weakened my immune system so that the bacteria could spread? Or perhaps the broad spectrum antibiotics I was given first in error (I was originally mis-diagnosed with tonsillitis instead of EBV) cased the bacteria to mutate into cell-wall deficient forms and/or form biofilms.
My specialist thinks the EBV caused the bacteria to spread, too, because it weakened my immune system. I just don't know...but one interesting thing, is that I have never had a high IgG for C. Pneum. before. I have been tested for yrs.....but after 8 months of antibiotics, it was suddenly high.
 

justy

Donate Advocate Demonstrate
Messages
5,524
Location
U.K
Hi Daffodil I also have Cpn, and Bartonella, but so far cant even take the antibiotics without adverse effects (as discussed on other threads) I know it is not from a clinical trial or scientific in any way but I have come across VERY many people with Lyme who after years of it go on to develop low levels of autoimmune antibodies (positive ANA). I asked KDM about my own Low titre ANA and he said so many of his patients with cpn have this...I cant begin to understand this, but just want o put it out there.
 

msf

Senior Member
Messages
3,650
Hi,

As someone with an intracellular infection that has been associated with auto-immune disease I thought I would take this chance to ask the good doctor about it.

I haven't looked into Hashimoto's disease much, but there does seem to be a correlation with Y. Entercolitica, and when I searched for the wrong Japanese disease I found that there is a suggested link with Kawasaki disease too.

I'm more interested in Reiter's Syndrome, though, as I seem to have had many of the symptoms of it, along with persisting IgG and IgA to Y. Enterocolitica. I would like to know what you mean by T-cell mediated rather than antibody-mediated, and why if that is true almost all the research has concentrated on the prolonged IgA antibody response rather than the T-cell response.

Also, as someone who knows the UK system, is there any way to see someone/get treatment for sub-clinical enthesitis?

Thanks,

Mark
 

msf

Senior Member
Messages
3,650
Oh, I obviously only know (a bit) about my case, but from what I've read the anti-smooth muscle auto-antibody can be produced as a result of both viral and bacterial infection of the liver.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
Hi,

As someone with an intracellular infection that has been associated with auto-immune disease I thought I would take this chance to ask the good doctor about it.

I haven't looked into Hashimoto's disease much, but there does seem to be a correlation with Y. Entercolitica, and when I searched for the wrong Japanese disease I found that there is a suggested link with Kawasaki disease too.

I'm more interested in Reiter's Syndrome, though, as I seem to have had many of the symptoms of it, along with persisting IgG and IgA to Y. Enterocolitica. I would like to know what you mean by T-cell mediated rather than antibody-mediated, and why if that is true almost all the research has concentrated on the prolonged IgA antibody response rather than the T-cell response.

Also, as someone who knows the UK system, is there any way to see someone/get treatment for sub-clinical enthesitis?

Thanks,

Mark

Yersinia causes Reiter's disease, as do various other intracellular bacteria. However, there is no evidence for specific immunity against self in Reiter's so it is not an 'autoimmune disease'. I have never heard of any reliable evidence linking these organisms to diseases with true autoimmunity in the form of autoantibodies like Hashimoto's. If there was such evidence I think I would have heard about it. Kawasaki is an odd one which as far as I know is not known to be autoimmune. The term autoimmunity has been very loosely used in the past which confuses everything.

The difference between T cell mediated and antibody mediated:
The adaptive immune system that produces specific immune responses to newly encountered antigens like viruses and bacteria and gives you 'memory' for such responses involves two main types of cell: T and B. Moreover, the T cells are divided mostly into CD4 and CD8.

The job of CD4 cells is chiefly to 'help' B cells make antibody to antigens floating about between cells. The interaction involves HLA-DR and DQ molecules, which is presumably why autoantibody production is often linked to certain DR or DQ genes. The diseases of this CD4 T dependent B response are the knwon autoimmune disease like lupus, RA, coeliac, scleroderma, pernicious anaemia etc etc.

The job of CD8 T cells is to recognise viral and bacterial antigens that have got inside cells. Since viruses always get inside cells CD8s are particularly relevant to virus immunity. CD8 T cells have their antigen presented to them by any cell, not just B cells, and this involves HLA-A,B and C, not DR and DQ. Diseases associated with A,B and C genes do not show autoantibodies or in fact any evidence of autoimmunity from the T cells but seem to involve a non-specific over-reactivity of T cells. They include ankylosing spondylitis and Reiter's (B27 linked) psoriasis and its arthritis (Cw6 and B27 linked) and Crohn's or UC arthritis (B27 linked). Behcet's disease is B51 linked but may involve the interaction of HLA-B with another type of cell - NK cells.

So as far as we know Reiter's disease is an over-enthusiam of CD8 T cells (which also like to talk to CD4 T cells but not B cells) that is not truly autoimmune. In almost all cases the bacterium that starts things off either dies off or is killed by antibiotic within two or three weeks. However, the T cells do not seem to settle down. This might seem odd but in Ank spond the T cells seem to get over-reactive without any involvement of bacteria so it seems that persistent overactivity is something that can occur anyway,especially if the B is B27.