The link between the microbiota or bacteria of our intestine and our brain is increasingly confirmed, as well as the impact of the microbiota on health. A recent study indicates that stress could negatively modify our intestinal flora and thus, increase the risk of developing autoimmune diseases.
Stress, changes in the flora and autoimmune diseases
Research recently published in the Journal of the American Society for Microbiology evaluated the mechanism by which stressful situations increase the risk of autoimmune diseases.
Thus, in mice exposed to social stress (encounters with aggressive mice) for 10 days and controls, the composition of the intestinal microbiota was evaluated. After the intervention, stressed mice had changes in the intestinal flora, especially in two types of bacteria related to immune disorders.
According to a genetic analysis of rodents, gut bacteria could become pathogenic and thus, harmful to the host itself.
A percentage of the gut bacteria in the stressed mice became pathogenic and infected their tissues, prompting the immune system to attack the body.
This was confirmed by tests on the lymph nodes of stressed rodents that indicate an increase in pathogenic bacteria and reactive effector T cells that are characteristics of autoimmune diseases such as lupus, multiple sclerosis, rheumtoid arthritis, scleroderma, among others.
Although this study allows us to recognize once again the close link between our emotions and brain with our intestine as well as the great power of the intestinal flora on our health, we must not forget that it was carried out in rodents and that might not be applicable to humans. Therefore, research is expected to confirm or bring us closer to the same link between stress, changes in intestinal flora and autoimmune diseases.
Likewise, it is always advisable to try to control stress in our lives as well as take care of the intestinal flora to protect health.
This article was originally published by Gabriela Gottau in July 2019 and has been reviewed for republication.
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