Arthritis breakthrough 'could stop crippling condition before it starts'
First study to prove gut
flora plays a role in rheumatoid arthritis
08:27 GMT, 13 June 2012
A breakthrough in our understanding of how rheumatoid arthritis develops could help scientists spot those at risk and even stop the condition before it starts.
Researchers have found that billions of bugs in our guts play a role in regulating the immune system.
The team from the Mayo Clinic in the U.S said that larger-than-normal populations of
specific gut bacteria may trigger the development of autoimmune diseases like
A GP examines a patient's hand for signs of rheumatoid arthritis. There are 400,000 sufferers in the UK
They could also fuel disease progression in people
genetically predisposed to the crippling and confounding condition.
'A lot of people suspected that gut
flora played a role in rheumatoid arthritis, but no one had been able to
prove it because they couldn't say which came first – the bacteria or
the genes,' said lead author Dr Veena Taneja.
'Using genomic sequencing technologies, we have been able
to show the gut microbiome may be used as a biomarker for
The findings from a study in mice could help scientists predict which people are more likely to develop the painful condition and stop it in its tracks.
Nearly one per cent of the world's
population has rheumatoid arthritis, a disease in which the immune
system attacks tissues, inflaming joints and sometimes leading to deadly
complications such as heart disease.
Although far less common that osteoarthritis, rheumatoid arthritis affects around 400,000 people in the UK.
Other diseases with suspected gut
bacterial ties include type I diabetes and multiple sclerosis.
This X-ray shows advanced rheumatoid arthritis of a 57-year-old woman. The condition is three times more common among women
Researchers with the Mayo Illinois
Alliance for Technology Based Healthcare say that identifying new
biomarkers in intestinal microbial populations and maintaining a balance
in gut bacteria could help doctors stop rheumatoid arthritis before
Dr Eric Matteson from the Mayo Clinic said: 'This study is an important advance in our understanding of the immune system disturbances associated with rheumatoid arthritis.
'While we do not yet know what the causes of this disease are, this study provides important insights into the immune system and its relationship to bacteria of the gut, and how these factors may affect people with genetic susceptibilities to disease.'
Dr Taneja and her team genetically engineered mice with a human gene that is a strong indicator of predisposition to rheumatoid arthritis. A set of control mice were engineered with a different variant of the gene, known to promote resistance to rheumatoid arthritis. Researchers used these mice to compare their immune responses to different bacteria and the effect on rheumatoid arthritis.
'The gut is the largest immune organ in the body,' said co-author Dr Bryan White, from the University of Illinois.
'Because it's presented with multiple insults daily through the introduction of new bacteria, food sources and foreign antigens, the gut is continually teasing out what's good and bad.'
The gut has several ways to do this, including the mucosal barrier that prevents organisms – even commensal or “good” bacteria – from crossing the lumen of the gut into the human body.
However, when good bacteria breach this barrier, they can trigger autoimmune responses. The body recognizes them as out of place, and in some way this triggers the body to attack itself, he says.
These mice mimic human gender trends in rheumatoid arthritis, in that females were about three times as likely to generate autoimmune responses and contract the disease.
Researchers believe these 'humanised' mice could shed light on why women and other demographic groups are more vulnerable to autoimmune disorders and help guide development of new future therapies.
'The next step for us is to show if bugs in the gut can be manipulated to change the course of disease,' Dr Taneja said.
The study has been published in the April 2012 issue of PloS ONE.