Recent research in the field of human microbiome studies are lending credibility to the notion that the human gut holds critical clues as to how Rheumatoid arthritis may be triggered and progresses. As research in the field continues and the scientific knowledge base grows, more will be added to this section.
[Gut Microbiota and Internal Diseases: Update Information. Topics: V. Gut Microbiota: Topics in Various Medical Fields; 2. Possible causal relationship of microbiota to rheumatoid arthritis and bronchial asthma]. Nihon Naika Gakkai Zasshi. 2015 Jan 10;104(1):71-4.
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Prevotella copri and the microbial pathogenesis of rheumatoid arthritis. Reumatol Clin. 2015 Mar-Apr;11(2):61-3. doi: 10.1016/j.reuma.2014.11.001. Epub 2014 Dec 30.
Mexican reviewer, Josè Moreno, discusses the complex nature of rheumatoid arthritis, it’s cause and progression, in light of historical and contemporary research findings. He points to the early 20th century origins of the theory for an infectious trigger, as well as subsequent failures in the ability to pinpoint one universal causal infectious offender. While he discusses infections, such as Porphyromonas gingivalis (P. gingivalis), mycoplasma, and Proteus mirabilis, his view is that recent research, pointing to an overabundance of Prevotella Copri microbes in the guts of new-onset rheumatoid arthritis (NORA) patients, relative to more beneficial Bacteroides bacteria. Although P. Copri isn’t a universal finding in all RA guts, he says it points to this gut microbe as being a strong contender for triggering RA due to its ability to drive Th17 development, a major inducer of joint damage in arthritis, similar to P. gingivalis. Further, he states that P. copri in NORA patients seems to be inversely-related to a shared etiope with this organism, inference being that it may be more important for patients with less susceptibility to a genetic predisposition to RA. Although there remain many unknowns with regard to this gut microbe, the hope is that further study will lead to targeted therapeutic options.
Rheumatoid arthritis: Prevotella copri associated with new-onset untreated RA. Nat Rev Rheumatol. 2014 Jan;10(1):2. doi: 10.1038/nrrheum.2013.187. Epub 2013 Nov 26.
A review of recent scientific findings of a high prevalence of Prevotella copri in the intestinal microbiome of rheumatoid arthritis (RA) patients and its implications.
A gut feeling about arthritis. Elife. 2013 Nov 5;2:e01608. doi: 10.7554/eLife.01608.
A Harvard reviewer discusses a multi-center, collaborative study by Scher, Littman, et al, conducted in the US, UK, Spain and Italy, discusses how the gut microbiome interfaces with many functions in the human body, from glucose metabolism, to nervous system functions, to circadian clock rhythms, and even to host immune defenses. This reviewer comments that it has long been accepted that healthy development of the immune system requires a healthy gut microbiome and it is becoming patently clear in contemporary research that aberrations in the gut microbiome can lead to the development of autoimmunity. She also states in conclusion that the work of Scher, Littman et all will open up new avenues to understand P. Copri, its mechanism of predisposing its host to autoimmunity and inflammation, and gut dysbiosis and raises the question that we still need to understand how arthriogenic signals, originating in the gut, result in joint disease.
Expansion of intestinal Prevotella copri correlates with enhanced susceptibility to arthritis. eLife. 2013; 2: e01202. doi: 10.7554/eLife.01202.
A multi-center collaborative study of 114 stool samples collected from rheumatoid arthritis (RA) patients, using the 16s rRNA gene sequencing method to identify intestinal bacteria by genetic coding. By studying the gut microbiome embodied in these samples, it enabled these researchers to conclude that new-onset RA (NORA) patients had an overabundance of Prevotella copri and a distinct lack of beneficial bacteroides. Further, by colonizing the guts of mice with P. copri bacteria, these microbes would dominate intestinal microbiota and led to greater susceptibility for chemically-induced colitis. The study authors believe that their findings identify a role for P. Copri in the pathogenesis of RA. This research also lends itself to the concept of novel treatments being developed to limit the growth of P. copri in the gut and, hence, delay or even prevent RA onset.
https://www.uab.edu/medicine/rheumatology/images/MS_-_Scher_et_al_2013.pdf