Researchers theorize that a certain type of gut bacteria triggers T cells to invade the eye. Now, they’re focusing on how to prevent that from happening.
Listen to your gut.
Because it turns out, your gut might affect your ability to see.
The National Eye Institute (NEI), a part of the National Institutes of Health, conducted a
Autoimmune uveitis occurs when a person’s immune system goes awry, attacking proteins in the eye. The study turned what was previously a mystery into the hypothesis that bacteria in the gut provides a training ground for immune cells to attack the eye.
“Activation could in theory originate in the eye itself, but since non-activated cells cannot go in and out of the eye at will, this is less likely,” senior study author Rachel Caspi, Ph.D., of the National Institutes of Health, told Healthline.
She said researchers eliminated most sources for the eye invasion. They finally honed in on retina-specific T cells that are activated in the gut.
“By the preponderance of evidence,” Caspi added, “the microbe explanation seems the most plausible.”
Autoimmune uveitis accounts for about
Corticosteroids provide a blanket approach to the disorder by suppressing the inflammation, but their long-term use can lead to adverse side effects.
By coming to an understanding of what triggers the disease, it opens the door for possible remedies for safer long-term health — or even preventing it, according to the NEI statement.
“These findings allow us to understand the biological basis for the disease,” Caspi explained. “The findings should in no way be interpreted that a patient can pop a probiotic pill and their disease will improve, or that they should start taking antibiotics to eliminate commensal bacteria.”
The eye is protected by a blood-tissue barrier that physically separates it from the rest of the body and minimizes the exchange of substances and blood-borne cells going in and out of the eye.
With autoimmune uveitis, T cells penetrate the barrier — but not before being activated.
T cells are preprogrammed to recognize proteins and target proteins on bacteria, viruses, and cells once they’re activated.
The proteins targeted in autoimmune uveitis are sequestered in the eye and don’t exist anywhere else in the body. That has left researchers dumbfounded on what activates the immune cells to allow them across the blood-ocular barrier.
“If indeed they can become activated in the intestinal tissue, this would explain how they are able to afterward enter the eye,” Caspi noted.
In the study conducted on mice, levels of activated T cells were not elevated in the lymph nodes (glands that swell during infections), but they were abundant in the intestines. This suggested that T cells may become activated in the gut before signs of the disease appear.
To test their theory, the researchers gave the mice an antibiotic cocktail designed to wipe out a broad spectrum of bacteria in the gut.
They found that mice without gut bacteria developed autoimmune uveitis much later and with less severity than mice with normal gut flora.
There was a similar delay in uveitis and decline in its severity when the uveitis-prone mice were raised in an environment free of bacteria and other germs. But when the same mice were later moved into normal housing, where they acquired normal gut bacteria, the uveitis appeared at full strength.
Caspi and the research team theorize the gut bacteria is similar to that in the retina, giving the T cells orders to look for that protein and attack it. Now, the key is finding which bacteria is the culprit.
“We are actively working on identifying the bacterium that could possess the protein which mimics the retinal antigen involved in our model of uveitis,” said Caspi, who added it’s a daunting task as many bacterial species come into play. “If found … we may be able in the future to use this knowledge to selectively eliminate the response that leads to the development of this disease.”
While the search for a way to eliminate or prevent the bacteria from attacking the retina is underway, Caspi said there’s no quick fix for the problem at this time.
“At this point we do not know which are the ones to target, but we do know that prolonged use of antibiotics can do more harm than good and leads to severe health complications,” Caspi said. “We obviously want to be able to prevent and cure all disease, but not all scientific discoveries that help us to understand the basic underpinnings of the disease are going to lead to a clinical solution in the foreseeable future.”