Bacteria living in the gut may contribute to the development of rheumatoid arthritis in people genetically predisposed to it, according to a study published in the journal Immunity.
This is because microbes stimulate a cascade of processes in the immune system that ultimately turns against the body’s own tissues – in this case against the joints. Our intestines are inhabited by thousands of species of bacteria, many of which are beneficial for the development of the immune system. However, the intestinal flora may also contribute to disturbances in the functioning of this system, especially its aggression on the body’s own cells. Recent research shows that this is what is happening with rheumatoid arthritis (RA), a serious disease that causes painful swelling and deformation of the joints and can lead to disability.
Scientists from the Faculty of Medicine at Harvard University and the University of New York have reached such conclusions by conducting experiments on mice predisposed to arthritis.
When rodents were reared in a sterile environment after birth, they had significantly less antibodies (immune proteins) in their blood to cause rheumatoid arthritis than normal animals. In addition, the onset and course of the disease were much milder.
In the third week of life, some of the mice were moved to microbiologically unclean rooms, and additionally, filamentous bacteria that normally inhabit the intestines were introduced into their bodies. Under these conditions, the animals began to produce specific antibodies and developed arthritis within four days.
In a sterile environment, mice did not develop joint disease, but introducing a single bacterium into the body was enough to initiate the immune processes leading to its occurrence, comments Diane Mathis, who participated in the study.
Of course, bacteria themselves are not the main cause of disease, emphasizes first author Hsin-Jung Wu. Rather, the point is that rodents have a genetic predisposition to arthritis, and bacteria create conditions for these predispositions to manifest themselves, the researcher explains. This is an example of the interaction between genes and the environment.
Closer analysis revealed that the bacteria stimulated the production of a particular population of T cells in the mice, which in turn signaled the B cells to produce antibodies to attack joint tissues as if they were foreign.
The researchers reminded that earlier studies showed that autoimmune diseases of the intestines, such as the irritable bowel syndrome, are related to the bacterial flora present in it. Surprisingly, however, gut bacteria can contribute to the development of an autoimmune disease that affects distant tissues such as joints.
In the future, scientists plan to continue their research, including to see if bacteria can also be involved in the development of other autoimmune diseases, such as type I diabetes (PAP)