Discovery Points to the Efficacy of Treating Genetic Eye Diseases with Antibiotics

A study by scientists from Germany and the United Kingdom could alter the treatment paradigm for certain hereditary diseases. Preclinical experiments have demonstrated a link between gut bacteria and genetic pathologies of the retina, which can lead to blindness. It was found that antibacterial therapy successfully addresses tissue damage, but now these results have led scientists to even more questions about the disease development mechanism.

Millions of people worldwide live with hereditary retinal diseases that can lead to blindness. A group of European scientists decided to explore the connection between the gut and eye diseases and discovered a rather unexpected result: despite a protective layer, bacteria often present in the eye tissue can provoke retinal diseases, reports Nature.

In the experiments, the well-known CRB1 mutation, which leads to retinal damage, was studied. Scientists created two mouse models with the CRB1 mutation, but in the first group, the rodents had a reduced level of gut bacteria. Observations showed that only in them did signs of retinal layer damage not develop, despite a genetic predisposition.

Moreover, antibacterial therapy reduced tissue damage.

“This allows us to suggest that patients with CRB1 mutations could benefit from using antibiotics or anti-inflammatory drugs that suppress bacterial activity,” stated co-author Richard Lee. Scientists now intend to assess the benefit of antibiotics in patients with this genetic defect. They need to evaluate the long-term effectiveness of such treatment. However, they are not yet sure that the therapy can reverse tissue damage. In parallel, the authors will continue to study the development mechanism of genetic diseases to trace all paths of retinal damage.

In another study, the dependency of infections on the gut was shown: scientists discovered a mechanism through which bacteria interact with immune cells in the lungs and protect the body from infections.

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