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#419481 - 11/11/10 10:33 AM Gut Bacteria Linked to Autoimmune Diseases
MollyC1i Offline

Registered: 01/21/04
Posts: 9813
Loc: Brittany, France (since Nov 08...
(Wendy has asked me to cross-post to here as well.)

(snip...) "Researchers have long associated periodontal disease, or gum inflammation, and bacteria in the gastrointestinal tract with RA, although no specific bacteria have ever been identified by researchers as the bacteria to target as possible therapy. Nevertheless, studies have suggested that bacteria or bacterial products contribute to RA and other autoimmune diseases." (more...)

(snip...) "The basic premise is that there are different oral and gut bacteria that activate Th17 cells to promote inflammation," Dr. Scher explains. "Our hypotheses are that characterization of Th17-inducing microbes in the human intestine will provide insight into disease pathogenesis, and that directed manipulation of the gut microbiota will result in the alteration of arthritis biomarkers, including Th17/Treg balance."

(snip...) "Additional studies by the group have demonstrated that specific microbes induce the differentiation of Th17 cells in the intestine. There is already strong genetic and therapy-based evidence that pro-inflammatory Th17 cells and anti-inflammatory regulatory T cells (Treg) have critical roles in autoimmune diseases, including RA, psoriatic arthritis, and Crohn's disease." (more...)

The next step for the team is a study in which 90 participants with RA will be subdivided into three arms. The first two arms will be given antibiotics for a two-month period, and the third arm will be given placebo. The researchers believe that by modifying the microbial flora with antibiotics, they can identify molecular mechanisms by which RA-associated bacteria affect Th17 and Treg homeostasis and thereby develop new strategies to diminish or even prevent the inflammatory process that leads to chronic destructive arthritis." (more...)

(snip...) "Conclusions: This is the first study using high-throughput technologies to assess oral and intestinal microbiota in RA. Our data corroborate prior reports demonstrating an underappreciated high prevalence of periodontal disease at a young age in patients with RA. Moreover, our preliminary data suggest that ACPA generation may be associated with larger populations of Prevotellaceae in both oral and intestinal microbiomes. In response to such altered microbial flora, certain predisposed individuals may develop auto-inflammatory disease, through mechanisms that may include the generation of cyclic citrullinated peptides or Th17 cell activation in the intestinal mucosa. Thus, the oral and intestinal microbiota merit further investigation as potential triggers for autoimmunity and clinical RA." (more...)

The American College of Rheumatology is an international professional medical society that represents more than 8,000 rheumatologists and rheumatology health professionals around the world. Its mission is to advance rheumatology. The ACR/ARHP Annual Scientific Meeting is the premier meeting in rheumatology.

Editor's Notes: Jose U. Scher, MD will present this research during the ACR Annual Scientific Meeting at the Georgia World Congress Center at 3:30 PM on Tuesday, November 9 in the Room A 411.

Would seem to reinforce Ebringer's seminal work...gut bacteria/inflammation - autoimmune diseases.
MollyC1i - Riding OutAS

#420299 - 11/16/10 12:09 PM Re: Gut Bacteria Linked to Autoimmune Diseases [Re: MollyC1i]
EricaK Offline

Registered: 06/23/10
Posts: 3845
Loc: Colorado, USA
Thanks for posting this. Bear with my thoughts on this... they're not very clear yet on this subject.

I've been wondering about the pain response vs. inflammation lately, and wondering if the pain response could be related more to a bacterial issue than to inflammation.

1. Many of us with USpD who experience super low inflammation and joint damage, but still suffer with periods of, or constant, debilitating pain.

2. There are people with negative arthritis tests who have super high inflammation and lots of joint damage, and internal damage to boot.

3. I've also been wondering if a third effect is the actual overgrowth of bone in people who are actively ankylosing and those with "only" osteo arthritis.

So, I've been wondering if the doctors have been wrong all along and that inflammation causes lots of damage, but does not actually cause the pain.

Maybe the disease, in combination with bacteria or some unknown other beastie, somehow (undiscovered as of yet) aggrivates the nerves, which cause pain, and in some prompts the body to react with inflammation IN ADDITION to the pain.

Well, I don't know if I've made any sense, but the current "pain comes from inflammation" only makes sense if one HAS inflammation. How do we explain severe pain that comes in the absence of inflammation?

I'm using myself as an example of this.
HLAB27+, RF+, ANA+, yet almost flat line CRP and ESR, even during periods of the most vicious pain. Could there be a bacteria or other pathogen that is causal?

Anyone else ever wonder about these things? confused2
ANA+ RF+ Rh- HLAB27+
Dx JRA 1967, GAD 1997, AS 2009, HMs 2010, CPS 2013
pulmonary edema w/ NSAIDS 2009

Movin' it so I don't lose it!

#420430 - 11/16/10 11:03 PM Re: Gut Bacteria Linked to Autoimmune Diseases [Re: EricaK]
Sue22 Offline

Registered: 01/13/08
Posts: 21341
Loc: Upstate NY
not commenting on your thoughts as i just don't know.

but i read something recently that made a lot of sense to me. its not that we don't have lots of inflammation, we do, its just that its all in the entheses, which are avascular, thus the blood inflammatory markers, ESR, CRP, don't show up due to the avascular nature of our disease.

this only helps to explain the spondys.

wendy had said that some RA patients also have low ESR and CRP. that i can't even begin to rationalize.

but that avascular nature of the entheses where all my inflammation resides makes a lot of logical sense to me.

as for pain, pain can also come from the muscle spasms, the fluid that comes with the inflammatory process, nerves being pressed on by the fluid, by the muscle spasms, etc.


Spondyloarthropathy, HLAB27 negative
Humira (still methylprednisone for flares, just not as often. Aleve if needed, rarely.)
LDN/zanaflex/flector patches over SI/ice
vits C, D. probiotics. hyaluronic acid. CoQ, Mg, Ca, K.
walk, bike
no dairy (casein sensitivity), limited eggs, limited yeast (bread)


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