Millions of people are affected by myopia (nearsightedness), in which they can see close objects clearly, but distance vision is blurred. Glasses, contact lenses or refractive surgery can improve vision, but don’t fix the underlying problem itself. But what if there were a way to address the actual cause of myopia?

OU College of Medicine researcher Jody Summers, Ph.D., a professor in the Department of Cell Biology, recently discovered that one of the body’s regulators of inflammation, a protein called Interleukin-6 (IL-6), plays a role in the development of myopia, thereby becoming a potential target to prevent or slow the condition. Summers published her findings in the influential journal eLife.

“The prevalence of myopia is increasing and is predicted to affect half of the world’s population by 2050,” Summers said. “With that increase, there is a greater likelihood that myopia will occur in people at a younger age. In some cases, myopia increases the risk of other serious eye conditions like retinal detachment, glaucoma and macular degeneration. Our study suggests that if we could target IL-6, it may be a means of controlling eyesight.”

Myopia typically occurs when the sclera (the white part of the eye) expands, causing the eye to be longer than normal. As a result, the light entering the eye is focused in front of the retina, instead of on the retina, resulting in blurry distance vision. That “defocus” also occurs when people wear glasses or contacts to correct myopia, but have blurry vision when they remove them.

Summers’ main focus for the study was on the choroid — the vascular layer between the retina and sclera — because molecules that could affect scleral growth are likely synthesized in the choroid or pass through it on their way to the sclera. She discovered that just at the moment of “defocus,” there was a rapid increase of IL-6 in the choroid.

“The increase in IL-6 is triggering a cascade of events that cause the eye to try to correct its size so that it is the right size for its focus,” she said. “Our hypothesis is that IL-6 is playing a positive role in that it detects when the eye is too long and then stimulates subsequent changes in an effort to get the eye to stop growing.”

The finding is important because once an action like that of IL-6 has been identified, researchers may be able target it with a drug in an effort to control eyesight. Summers is the first researcher to demonstrate the association between IL-6 and eye size. IL-6 is a cytokine, a type of protein that regulates inflammation in the body. It is released by muscle cells during exercise, when people have a fever or become injured, and, more recently, in those who are battling the “cytokine storm” involved in COVID-19.

“Researchers hadn’t been thinking about myopia as an inflammatory process; we thought of it more as a neural process,” Summers said. “But in this case, IL-6 seems to be playing a role.”

Summers also made an ancillary finding concerning atropine, the drug used to dilate pupils. Atropine is being studied around the world as a potential treatment for myopia. When Summers used atropine in her investigations, IL-6 again increased, suggesting that the positive effect of atropine in slowing eye growth was due to increased IL-6 in the choroid.

While her findings are promising, there is much more work to be done, Summers said. She plans to continue replicating her findings and to develop a way to control IL-6 directly in her experiments.

“This is exciting because it may give us a new way of approaching myopia,” she said.

Summers received a bridge grant from Oklahoma City-based Presbyterian Health Foundation, which allowed her to earn the National Institutes of Health award that funded this project.