Dysbiosis of the gut microbiota may be linked to the development of rheumatoid arthritis (RA), according to a team of researchers.
What is rheumatoid arthritis?
RA is a chronic inflammatory disease affecting the joints. It is an autoimmune disease that progresses in flare-ups. Thus, the antibodies produced by the body will attack the synovial membrane of the joints.
RA is characterized by joint deformation and destruction, joint pain, swelling and inflammation. It is a multifactorial disease, dependent on environmental, hormonal, immunological and genetic factors, although the exact origin of the disease is still unknown. However, a new component seems to interest researchers: the intestinal microbiota.
A new hypothesis
Considerable interest has focused on dysbiosis of the gut microbiota as a possible driver of disease.
This new study envisages a correlation between the severity of the disease and damage to the intestinal wall caused by certain bacteria.
In other words, changes in the gut environment are potentially responsible for the pathogenesis of the disease.
Studies carried out to link intestinal permeability and rheumatoid arthritis
Through studies on mice and patients with RA, the researchers found that differences existed between healthy subjects and those with the disease.
The results in mice showed that:
- Those bred to have a genetic predisposition to intestinal permeability developed signs of severe arthritis.
- Those with collagen-induced arthritis had reduced joint swelling when gut permeability was improved.
The results of the clinical study complement these observations. Compared to healthy people, RA patients had higher blood levels of markers for intestinal damage and permeability. These include LPS (lipopolysaccharide), LPS binding protein and intestinal fatty acid binding protein, which are markers of intestinal damage and permeability. The researchers also report that levels of LPS-binding protein are also related to disease severity.
Microbiota: future therapeutic target for rheumatoid arthritis?
The intestinal mucous lining would therefore be deeply damaged in the case of arthritis and would no longer play its barrier role properly. This type of injury would lead to an accumulation of white blood cells in the intestine causing inflammation. Bacteria are then able to pass through the intestinal wall.
These results offer hope for the development of new strategies to treat this disease. However, this study does not fully describe the mechanisms that may explain this relationship. Further studies should be considered.
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