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Interview: Ian Lipkin’s Million Dollar Appeal for Microbiome Study

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Simon McGrath recently secured an interview with the world famous Dr Ian Lipkin – a scientist who continues to believe that ME/CFS has a physical cause – to discover more about his plans for a major study of the gut microbiome and to find out why he's asking the patient community for its support…


Dr W. Ian Lipkin has demonstrated a clear commitment to ME/CFS research. First came his study looking at Borna virus in the 1990′s, and then the landmark study that ruled out XMRV as a cause, and most recently we have heard about the huge pathogen and immune study – a vast collaboration with many key clinicians and researchers, including Dr Dan Peterson and Professor Jose Montoya.

That research had already found clear signs of immune activation in patients and, when I spoke to him, Lipkin was clearly excited about the very latest results to emerge from the study - I wish I could reveal more, but a paper has just been submitted and details are embargoed until publication.

Lipkin believes that immune activation may be responsible for driving the symptoms associated with ME/CFS. And that the immune activation and could itself be triggered by bugs, not in the blood, but found in the vast ecosystem of bacteria, viruses and fungi, that constitute the gut microbiome.

However, he doesn’t have the funds to pursue this research and so he’s appealing to the patient community for the one million dollars he needs to get the work done. The payoff? A better understanding of the illness and the possibility of new treatments.

Dr Lipkin on ME/CFS

Lipkin made a splash in the world of ME/CFS when he led the XMRV study that both disproved its role in the illness and also managed to unite the patient community. At the press conference for that study he said his first brush with CFS was a large study in the 1990s that demonstrated no connection between the Borna virus (one of many viruses he’s discovered) and CFS. But he stressed that their findings in the same study of B-cell activation in CFS patients was a clear sign that this was not a psychosomatic disorder. The findings in his new study have only confirmed his views:

“There is no question in my mind that this is a physical disorder. The fact that we haven‘t been smart enough or invested enough in it to sort that, doesn’t mean that this is anything else.”

The smoking gun

The immune activation he’s found could explain fatigue – it’s almost a universal symptom of infections like flu, and is actually a consequence of immune activation rather than caused by pathogens themselves.

The same could be true of other ME/CFS symptoms including disturbed sleep and brain dysfunction which again are typical symptoms of immune activation.

Lipkin is eager to build on this work. He believes the immune activation is a smoking gun and now wants to track down who or what pulled the trigger.

“I am more keen than ever … to see if we can identify the trigger”
- all quotes are from Dr Lipkin

There are several credible places to look for the culprits triggering the activation. One is white blood cells: some viruses could be hiding out in cells and so wouldn’t have been found by the initial search in the blood plasma – and Lipkin already has a white blood cell study lined up.

However, his attention is particularly focused on the microbiome, the large ecosystem of bugs that live on our skin and within our ‘inner tube‘ that leads from mouth to bottom.

There are at least one trillion bugs in the gut microbiome – and there are more immune cells in the gut than anywhere else: it’s a great place to hunt for bugs that might be triggering immune activation.

Microbiome problems are increasingly being linked to serious illness. The most striking example is the superbug Clostridium Difficile (C. diff), which has become a major problem in hospitals. C. diff lives in most of our guts harmlessly at low levels, but it can take over (particularly if ‘good’ bacteria are killed off) – causing diarrhoea and even death. Happily, doctors have discovered that severe C. diff cases can be treated relatively easily by restoring the microbiome; unhappily, this involves a faecal transplant.

The potential to treat disease by restoring the microbiome is one reason this area of research is attracting so much attention. This recent article explains more about the microbiome, how it might link to ME/CFS and looks at other research being performed.

“If the answer were simple, it would be done by now”

Irritable Bowel Disease is another example – here inflammation is believed to result from changes in the microbiome. Lipkin’s team have just been studying women in sub-saharan Africa and found that certain bacteria in the vaginal microbiome increase the risk of HIV infection. Lipkin thinks the gut microbiome could be playing a similarly important role in ME/CFS:

“By analogy with animals and human situations, we see that different populations of fungi, bacteria and viruses in the colon can have an impact on the immune system and give rise to cytokine activation which could cause the symptom complexes we see in ME/CFS”

in other words:

changes in microbiome > immune activation > symptoms of ME/CFS

I asked Lipkin if this meant particular bugs causing inflammation and he said that is certainly possible. But, he added, another route to illness is that an overgrowth of ‘’bad’’ bacteria could form a film, preventing ‘’good’’ bacteria from interacting positively with the immune system (see this article for more) – an indirect way of causing immune dysfunction.

The exact role that microorganisms in the gut play in health and in the development of disease is complex and still being determined. There are many plausible hypotheses, says Lipkin, and only research can show which (if any) are right.

If the microbiome is the cause, is it treatable?

If the microbiome is the cause (or a cause, or even a contributor) of ME/CFS, it might be relatively easy to treat, perhaps with probiotics, restriction diets, drugs, or even faecal transplants.

Cause or effect?
Of course, the first step in this process is demonstrating a strong link between the microbiome and ME/CFS. If one is found then the next step is to look for evidence it plays a causal role: i.e. do microbiome changes cause immune dysfunction, as opposed to being a consequence of or simply associated with immune dysfunction?

Lipkin says one option is to use an animal model: the idea would be to introduce the microbes suspected of triggering ME/CFS into the gut microbiome of animals, to see if this leads to similar symptoms and immune activation as seen in humans. Something that has been used to study Metabolic syndrome.

Personalised medicine
If there is evidence of a causal role, Lipkin says they would look to establish clinical trials of treatments that could include probiotics, antibiotics followed by prebiotics, restriction diets and possibly even faecal transplants. He believes that there would not be a single microbiome cause of the illness, but different types – potentially fungal, bacterial and viral problems causing three separate types of immune dysfunction.

Lipkin calls these different types ‘endophenotypes’ and it could lead to personalised medicine, where the particular treatment depends on the specific form of the illness. There will be endophenotypes beyond those in the gut, such as genetics endophenotypes, and it is highly unlikely that the microbiome would account for all forms of ME/CFS – but this approach could tackle a very substantial proportion of cases.

The study breakdown

Lipkin’s proposed study will look at all three trees of life: bacteria, fungi and viruses in the microbiome of 100 patients and 100 controls recruited for a previous NIH study. It will cost a cool million dollars:

1. Sample collection: $150,000
Collection of faecal (and blood) samples from patients, including checking the initial ME/CFS diagnosis remains valid and shipping chilled samples back to the labs at Columbia.

2. Faecal Microbiome sequencing and Analysis: $317,000
- Separate, purify and perform high-throughput sequencing of viruses, fungi and bacteria
- Complete sequencing of viruses; partial sequencing to identify bacteria (using 16S rRNA) and fungi (using ITS, the ‘fungal barcode’)
- Generate microbiome profile for each patient, one each for bacteria, fungi and viruses​

Comparison of patient and control microbiomes: bacteria, fungi and viruses that differ in prevalence between CFS subjects and controls will be considered candidates for contributing to either health or disease.

3. Development of highly-accurate real-time PCR assays to confirm findings and levels of microbes: $328,000
This will quantify how much there is of each bug of interest (the main high throughput sequencing approach gives an indication of quantity but is less accurate than real-time PCR).

It’s possible, that the most important thing isn’t the presence or absence of a microbe, but the amount of it – as with C.Difficile. These assays will also be used to check that key microbes haven’t been missed in any patient or controls who were negative for them in initial sequencing, as PCR assays are far more sensitive than high-throughput sequencing.

4. Cytokine analysis: $86,000
The study will again measure cytokines in blood and undertake data analysis to see if there is an association between cytokine profiles and immune profiles. It would then provide strong evidence of an important relationship between the microbiome and immune dysfunction – the hypothesis driving this study. Sophisticated analysis will be required on the vast amount of data generated by microbiome and cytokine profiling; happily, Lipkin’s Center for Infection and Immunity have a team of biostatisticians dedicated to such work.

5. Development of antibody tests for important bugs identified by the microbiome work: $249,000
It could be a few individual species or particular groups of microbes, but antibody tests will be developed by Lipkin’s lab to allow much easier testing to see if the same problems in this sample are found in the wider patient population.

As well as guiding treatments, the PCR assays and antibody tests developed here could both provide a diagnostic test for ME/CFS.

Lipkin’s record



Featured in the New York Times, described by Discovery magazine as the world’s foremost virus hunter, and consultant to a successful Hollywood movie, Dr W. Ian Lipkin has a higher profile than most researchers. But this profile is built on a stellar scientific reputation.

He’s discovered more viruses than anyone else. He’s part of the World Health Organization (WHO) diagnostic discovery and surveillance programme designed to catch pandemics as they arise. And the Chinese recruited him play a leading role in their fight against SARS.

Amongst other things he is John Snow Professor of Epidemiology and Director, Center for Infection and Immunity at Columbia University. Full biography.

He is passionate about communicating science to a wider audience but is insistent the science is right.

Lipkin only agreed to consult on Contagion, a movie about the terrifying potential of epidemics, because of director Steven Soderbergh’s desire to make a film that was true to the science – having turned down offers to advise on several movies with somewhat wilder plots.

When Lipkin was shown a near-final version of the film he threw up his hands at the scene near the climax where a scientist injects herself in the leg with the new vaccine, through her tights – a poor practice that could easily introduce an infection.

This might seem a small detail given everything else the film had right, but Lipkin was adamant it had to go: cue a $100,000 reshoot.

This near-obsession with getting things right is a Lipkin hallmark. The very first point he made to me about this study, before discussing any details, was the need for real, robust findings – because there have been too many false dawns in this field.

At the end of the interview he emphasised the need of crisp, rigorous data. Whatever the findings from this new study – positive or even negative, we should be able to rely on them.​


Scientist in a hurry for answers

Dr Lipkin is a scientist in a hurry for answers. That’s true both in his work trying to stop a new pandemic in its tracks, and in his work on ME/CFS.

He wants to follow up as many promising leads as possible, as soon as possible – rather than waiting for the results of a single study before planning a new one if the first draws a blank.

That’s why he set up a huge study looking for specific pathogens such as EBV, but also used deep sequencing alongside that to search for any other pathogen, known or unknown.

He’s looked in blood plasma for pathogens but is also about to look for them in white blood cells too.

He set the study up to look at immune markers including cytokines as well as for pathogens – and the significant findings of immune activation show the value of backing more than one horse.

On top of all this, Lipkin has invested in a gene expression study using samples from the same study, with results expected shortly that could throw up new leads in epigenetics and genomics.

Dr Lipkin has committed a huge amount of his 60-strong institution’s time to pursuing numerous studies, all aiming to uncover what’s really going on in ME/CFS

Too much, too soon?
However, it may be that the NIH is not in such a hurry as it has declined to fund the study at this time.

But then the NIH has only ever committed relatively small amounts of funding to ME/CFS – around $5 million a year, compared with around $115 annually for MS and $284m for Asthma.

Its funding record firmly suggests the NIH’s priorities lie elsewhere.

So, as Lipkin says, “we are stuck”. It’s possible that the NIH will fund this work in the future, and possible they won’t.

The question is, do we want to wait?

“We are already well behind where we should be”

Dr Lipkin has now appealed to patients to fund his latest study that aims to hunt in the gut microbiome for the ‘trigger’ of the immune activation his study found in ME/CFS. And he needs a cool million dollars to pay for the study outlined above.

Actually, the study comes to a bit over a million dollars (see above) - $1.13 million, to which another $140,000 of costs for maintaining the high-tech equipment used and general lab costs making $1.27 million in total. However, the initial target has been set at $1 million.

In his CDC telecast to patients last September, Lipkin explained the microbiome project was being held up by this lack of funds, and urged patients to contact their representatives in Congress.

He also appealed directly to patients who could afford to do so, to invest in research:

“it may not be appropriate to pass the hat, but that is exactly what I am doing”

How long will it take for the results? “Within a year”, said Lipkin

The man is in a hurry, and the study is all set up and ready to go – once funding is available.

“As long as I can do it, I will do it. I‘m eager to start, I‘m optimistic it will bear fruit, it‘s not just an academic exercise, it could lead to treatment”
When I mentioned to Dr Mady Hornig, the Principal Investigator on this study, that I was interviewing Dr Lipkin she added: “Terrific – we need the resources to get this done”.

Crowdsourcing: Together we can make it happen

I do think we are very lucky to have Dr Lipkin on our case and believe that we should back his new study, which will be performed at his Center for Infection and Immunity, Columbia University – the world’s largest and most advanced academic center in microbe discovery, identification and diagnosis.

“Why don‘t we crowdsource this, we are all losing valuable time in our lives?”
Vanessa Li, Phoenix Rising member and fundraiser

ME/CFS patient, Vanessa Li, responded to Lipkin’’s call last year, by contacting his office and suggesting crowdsourcing in a similar way to MEandYou, which through the efforts of Dr Maria Gjerpe had raised an astonishing $0.5 million towards the Norwegian Rituximab trial in 90 days.

Lipkin was a physician in San Francisco at the start of the AIDS epidemic and commented how, when the government was reluctant to pay, much of the important early work was funded by private donors so he’s very open to this possibility. He continued to seek funds for his work from institutions, but as that hasn’t worked he is now asking patients if they can make the study happen - and has given this interview to launch the million dollar appeal.

Donate to the the ME/CFS microbiome study
I have just donated and hope many other patients will do too. Just click on the button below and follow the instructions. The option is to donate to CFS research, but in the next page you can add ‘special instructions’ such as ‘for the microbiome study’.

We need only for every US patient to donate $1. Or one in ten patients to donate $10.


If people want to do more to help – and this is a big target – they can help to promote this crowdsourcing initiative at this new group, or email Vanessa Li. I will give her the last word:

The CDC says there are more than one million ME/CFS patients today in the US alone. There is no reason why, if every patient were made aware of Dr. Lipkin’s appeal and donated $1, that we should fail to raise the $1 million. An esteemed researcher doing high-caliber work is taking a serious interest in finding out the cause of our desperately under-researched illness. Now is the time to act!​

Simon McGrath tweets on ME/CFS research:


Phoenix Rising is a registered 501 c.(3) non profit. We support ME/CFS and NEID patients through rigorous reporting, reliable information, effective advocacy and the provision of online services which empower patients and help them to cope with their isolation.

There are many ways you can help Phoenix Rising to continue its work. If you feel able to offer your time and talent, we could really use some more authors, proof-readers, fundraisers, technicians etc. and we’d love to expand our Board of Directors. So, if you think you can help then please contact Mark through the Forum.

And don’t forget: you can always support our efforts at no cost to yourself as you shop online! To find out more, visit Phoenix Rising’s Donate page by clicking the button below.


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Comments

We are I think able to confirm that we should have our primary plaforms - website and Facebook pages and twitter feeds - launched before the US conferences begin 19/20 March at which both Montoya and Lipkin et al will all be presenting. Hopefully, the presentations and interviews, will provide a boost to the campaign efforts so we wanted to ensure the platforms were in place by then...
Thank you, Firestormm, that was exactly what I was hoping for. Thanks to everyone for their work on this.
 
Our disease is NOT caused by Lyme, mold, herpes viruses, gut bacteria, or anything these specialists are trying to look for and treat. These are infections our bodies should be able to control.

It is AUTOIMMUNE. see the new paper: Transcriptional de-repression of ERVWE1 following influenza A virus infection.

Again, the ONLY researcher I am aware of, who is looking at this factor, KDM/Lombardi/WPI.

Why do we continue to support the search for pathogens? I find this very frustrating.

Of COURSE we will have pathogens, gut inflammation, differences in gut flora. This is a given.

I urge you to support those who are narrowing in on the true cause.

some HIV drugs helps some people because they act on HERV. Ampligen helps some people because it makes us produce interferon, so our bodies can again control the infections.

I am so scared that these pathogen studies will be more of a waste of precious time some of us do not have.
KDM presents a brand new cause of ME every year, each time discarding his old one. Last year it was Lyme, now it is the flu. Sorry, but no. There is no reason to abandon all other research because KDM has found another small anomaly, not even in ME patients.

The erroneous immune response in ME can be explained by latent herpes viruses keeping differentiated B-cells alive for their own survival, thus hindering the immune system's flexibility to deal with a new, enteroviral infection.

This model has stood unrefuted for 25 years but it needs confirmation.
 
We are I think able to confirm that we should have our primary plaforms - website and Facebook pages and twitter feeds - launched before the US conferences begin 19/20 March at which both Montoya and Lipkin et al will all be presenting. Hopefully, the presentations and interviews, will provide a boost to the campaign efforts so we wanted to ensure the platforms were in place by then...
Thank you, Firestormm, that was exactly what I was hoping for. Thanks to everyone for their work on this.
vli, thank you for the updates on the progress of the fund-raising!

Firestormm, thank you for all your efforts that you describe in your March 2 post.

Daffodil, to me it seems remarkably close-minded to categorically state that "it is autoimmune" and dismiss any of the other factors that you listed. It is entirely possible that, in some patients, some kind of pathogen in the gut is throwing the immune system out of whack. Please try to keep an open mind and not dismiss the efforts of scientists and researchers who know a lot more than you and I do about the intricacies of the human body. Thanks.

Drew
 
lol ok fair enough. i do tend to get carried away with my flavor of the month. but keep in mind Lombardi has done tissue studies using next generation sequencing already....
 
Hi All

I've just today received a very nice 'thank you for your donation' letter from Columbia University (cc'd to Dr Lipkin).

If Ian Lipkin manages to 'crack' ME/CFS these letters could be a little piece of history (OK unlikely to become collectable if we hopefully get donations by the thousands).

So come on - get to say I was part of this!:)

@Firestorm et al. Just a small point - nice as it was to get this letter I couldn't help noticing that the postage was over a dollar that would have been better kept for the study. I don't know if PR members are in direct contact with Columbia or what its policy is (or is it a tax deduction thing) but perhaps thank you letters could be restricted to big donors?
 
Hi @Marco - I also got a letter from them today thank me for my donation and wish I'd kept the envelope to see what it had cost.

We'll be approaching them about that letter - we can see some potential for it helping to build the campaign - and that's a good point about cost. An email might be more appropriate for many donations.

:thumbsup:
 
Hey @Sasha

We both have our names on the same sheet of paper as Ian Lipkin's.

Bet he's chuffed ;)
 
Hi All

I've just today received a very nice 'thank you for your donation' letter from Columbia University (cc'd to Dr Lipkin).

If Ian Lipkin manages to 'crack' ME/CFS these letters could be a little piece of history (OK unlikely to become collectable if we hopefully get donations by the thousands).

So come on - get to say I was part of this!:)

@Firestorm et al. Just a small point - nice as it was to get this letter I couldn't help noticing that the postage was over a dollar that would have been better kept for the study. I don't know if PR members are in direct contact with Columbia or what its policy is (or is it a tax deduction thing) but perhaps thank you letters could be restricted to big donors?
I'm pretty sure that postage comes out of a different 'pot' to the microbiome study so won't make a difference - and this way everyone gets their little bit of history :)
 
Hi @Marco - I also got a letter from them today thank me for my donation and wish I'd kept the envelope to see what it had cost.

We'll be approaching them about that letter - we can see some potential for it helping to build the campaign - and that's a good point about cost. An email might be more appropriate for many donations.

:thumbsup:
Yes, it can be very annoying when part of your donation is wasted with a snail-mail acknowledgement. I actually stopped participating in the regular prize draws for one charity because it kept sending thank-you letters. I emailed them about it, and put notes on my entry form, and even ticked the 'no acknowledgement' box on the entry form when they started including these. I still got acknowledgments! :bang-head: My donations were not meant to go to the mail service!
 
I too received a thank you letter. My first reaction was that it was a waste of one dollar and ten cents for the postage but then I realised that I got a fuzzy feeling (don't often get them!) from the letter which will probably make me try to send the next ten dollars sooner than I'd planned :)
 
I'm pretty sure that postage comes out of a different 'pot' to the microbiome study so won't make a difference - and this way everyone gets their little bit of history :)
Dammit Simon. You're using that ...... LOGIC thing!

Absolutely right - its bound to be coming out of a central admin budget which would explain the cc'ing to Lipkin.
 
FYI: The NIH has allocated $715 million dollars to the Human Microbiome Project.
http://hmpdacc.org/
https://img.jgi.doe.gov/cgi-bin/imgm_hmp/main.cgi?section=FindGenomes&page=findGenomes&domain=all
http://hmpdacc.org/tools_protocols/tools_protocols.php

Funding has been given to numerous institutes to investigate microbiome in various diseases.
https://www.bcm.edu/departments/molecular-virology-and-microbiology/cmmr/index.cfm?pmid=23880

You would think they could chisel off $1 million for ME/CFS.
 
I just wanted to highlight an article written towards the end of last month, that was sent to me the other day. It is about a study that used similar technology on the microbiome as Lipkin will in his own proposal that we are raising funds for him to begin.

We did discuss this paper when it came out last year. You can read Simon's comments HERE for example and their bearing on Lipkin's work, and also a comment from Professor Edwards HERE. All findings need replication of course, and that will include anything Lipkin finds and creates a theory from. Such is the nature of science.
Shifts in the Microbiome Cause Rheumatoid Arthritis

A new study suggests that intestinal expansion of Prevotella copri may be associated with the pathogenesis of RA

by By Lara C. Pullen, PhD (published Feb. 20, 2014)

[These are extracts from the article]

Jose U. Scher, MD, director of the Arthritis Clinic at New York University Hospital for Joint Diseases in New York City, and colleagues describe the results from their stool-sample analysis in eLIFE.1 The team compared the genome sequence of gut bacteria from patients with RA to those from healthy controls.

“Despite impressive advances in RA pathogenesis, diagnostics, and therapeutics, the etiology of this disease remains elusive. For many decades, gut bacteria have been implicated in inflammatory arthritis. Using novel technologies that help bypass the need for classic cultures, we have been able to describe an association of a particular species P. copri with an autoimmune phenotype,” says Dr. Scher.

“Multiple lines of investigation are focusing on various strategies, including bacteriotherapy (fecal transplant), probiotics, probiotics and bioactives (targeting molecules produced by gut bacteria),” says Dr. Scher. He acknowledges that more studies are needed. That said, Dr. Scher’s work suggests that treatments that focus on curbing the spread of P. copri in the gut may delay or prevent the onset of RA."
 
I just wanted to highlight an article written towards the end of last month, that was sent to me the other day. It is about a study that used similar technology on the microbiome as Lipkin will in his own proposal that we are raising funds for him to begin.

We did discuss this paper when it came out last year. You can read Simon's comments HERE for example and their bearing on Lipkin's work, and also a comment from Professor Edwards HERE. All findings need replication of course, and that will include anything Lipkin finds and creates a theory from. Such is the nature of science.
Seemed interesting until I looked at the article and found that it relates to a study on MICE.

So, there is perhaps a 50% chance that the findings are relevant to humans.

I have posted an article giving some info about mouse 'models' of the human gut here.

Similar problems will apply to other animal 'models'.

The details of the human research are only of 'associations'. These do not tell us anything about causality.

I do subscribe to the hypothesis of the microbiome being involved in the causal chain of autoimmune disease, but personally doubt whether one particular microorganism is of significant importance. A range of differences has been found between the gut flora of healthy subjects and those of autoimmune patients. The real issue may be the balance rather than specific microorganisms.
 
@MeSci You must be (and I know what you are going to say) rather pleased that at least Lipkin is looking in humans for the bugs in the first instance.

The thing with RA was that - and from what I have understood - the association with the microbiome had been made in humans and then they took it to mice models. It may be that Lipkin will do similarly - as was said.

I know you feel strongly about this, and I agree that seeing something in mice, doesn't mean the causal mechanism or pathways can be replicated in humans. But first things first I think. Let's hope Lipkin and his team can find some bugs and proliferation that are noticeably different in patients than in controls and then we can see what the next stage might be.

I think this is going about it the right way - foundations first and all that. Then commeth the theories and the further testing of them. And then we might one day learn if something in the microbiome can be tied to this immune activation that is increasingly being seen and reported on.

The microbiome is I think a necessary 'frontier' for ME research and I am pleased to support this study, whilst acknowledging it cannot hope to be the final word on the subject and that other scientists will - and are - carry out their own research.

NIH Research Matters: November 25, 2013

Gut Microbes Linked to Rheumatoid Arthritis

"...To see if these microbes might also be associated with rheumatoid arthritis in humans, Dr. Dan Littman of NYU School of Medicine led a team of researchers that examined DNA in 114 stool samples from both healthy people and those who had rheumatoid or psoriatic arthritis.

The team identified gut bacteria by extracting DNA from the samples and then analyzing a bacteria-specific gene called the 16S ribosomal RNA gene.


The research was funded in part by NIH’s National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institute of Allergy and Infectious Diseases (NIAID), and National Human Genome Research Institute (NHGRI). Results appeared online on November 5, 2013, in eLife.

The researchers found that 75% of people with new-onset, untreated rheumatoid arthritis had the bacterium Prevotella copri in their intestinal microbiome.

In comparison, it was present in 12% of people with chronic, treated rheumatoid arthritis, 38% of people with psoriatic arthritis, and 21% of those in the control group.

Increased levels of P. copri correlated with reductions in several groups of beneficial microbes, such as Bacteroides. The researchers performed more complete DNA sequencing on a subset of samples and identified unique Prevotella genes that correlated with rheumatoid arthritis.


To test whether P. copri could influence inflammation, the team administered the bacteria to healthy mice so that the bacteria became part of their gut microbiome.

Mice were then given a chemical that inducedcolitis, a model of gut inflammation. Animals with P. copri developed more severe symptoms than the mice that hadn’t received the bacteria. The finding provides further evidence for a potential role for P. copri in inflammation...."