NIH study shows microbe living on the surface of the eye protects cornea from infection.
Resident microbes living on the eye are essential for immune responses that protect the eye from infection, new research shows. The study, which appears in the journal Immunity on June 27, demonstrates the existence of a resident ocular microbiome that trains the developing immune system to fend off pathogens.

For years, the ocular surface was thought to be sterile because of the presence of an enzyme called lysozyme that destroys bacteria, antimicrobial peptides, and other factors that rid the eye of microbes that may land from the air (or from our fingers) onto the surface of the eye.

Anthony St. Leger, PhD, research fellow in Caspi’s laboratory, was able to culture bacteria from the mouse conjunctiva, the membrane that lines the eyelids. He found several species of Staphylococci, which are commonly found on the skin, and Corynebacterium mastitidis (C. mast). But it wasn’t clear whether those microbes had just arrived on the eye and were en route to being destroyed, or whether they lived on the eye for extended periods of time.

The researchers found that C. mast, when cultured with immune cells from the conjunctiva, induced the production of interleukin (IL)–17, a signaling protein critical for host defense. Upon further investigation, they found that IL–17 was produced by gamma delta T cells, a type of immune cell found in mucosal tissues. IL–17 attracted neutrophils to the conjunctiva and induced the release of anti–microbial proteins into the tears. The researchers are currently investigating the unique features that can make C. mast resistant to the immune response that it itself provokes and allow it to persist in the eye.

To determine whether the microbe was contributing to the immune response in mice, St. Leger formed two groups, one control (with C. mast) and one treated with an antibiotic to kill C. mast and other ocular bacteria, and then challenged them with the fungus, Candida albicans. The mice receiving antibiotics had a reduced immune response in their conjunctiva and were not able to eliminate C. albicans, leading to full–blown ocular infection. The control mice with normal C. mast on the other hand were able to fend off the fungus.

When inoculated with C. mast, JAX mice produced conjunctival gamma delta T cells that released IL–17. Bacteria could still be cultured from their eyes after many weeks. By contrast, several other strains of bacteria inoculated onto the eyes of JAX mice disappeared without inducing local immunity. “We still don’t know what enables C. mast to successfully establish itself in the eye, whereas other similar bacteria fail to colonize,” Caspi said.

Interestingly, C. mast was not spread to cage–mates even after eight weeks of co–housing; however, C. mast can be passed from mother to pup. Both of these observations support the notion that C. mast is a resident commensal, not a bacterium that is continually re–introduced to the eye from the skin or the environment, Caspi explained.

Although C. mast appears to stimulate a beneficial immune response, there may be situations in which it could cause disease, St. Leger noted. For instance, the elderly tend to have suppressed immune systems, which might allow C. mast to grow out of control and cause disease.