Bacteria breach barriers to enter eye

March 14, 2012

Scientists from the Schepens Eye Research Institute have discovered how a bacterial pathogen can break down the protective molecules on mucous membrane to enter and infect a part of the body.

Boston-Scientists from the Schepens Eye Research Institute have discovered how a bacterial pathogen can break down the protective molecules on mucous membrane to enter and infect a part of the body.

In a study published in the March 7, 2012, PLoS ONE, the researchers describe how they discovered that an “epidemic” strain of Streptococcus pneumoniae, which causes conjunctivitis, secretes an enzyme to damage the protective molecules, called mucins, and breach the mucosal membrane.

“Our discovery may ultimately lead to new ways of diagnosing, treating, and preventing bacterial infections originating not only in the eye but in other parts of the body as well,” said Ilene Gipson, PhD, the study’s principal investigator and a senior scientist at the institute.

The outer surface of mucous membranes are protected by two types of mucin molecules: one that is secreted and is in constant motion to sweep away trapped foreign material from the membrane surface, and another that remains rooted in the membrane surface. The latter type of mucin molecules constitute a physical shield that keeps potentially harmful substances from penetrating the membrane.

These membranes often encounter two types of bacterial pathogens: opportunistic pathogens that sit on the membrane surface and only enter the tissue when trauma or injury leaves a gap in the mucous membrane layer, and non-opportunistic or epidemic pathogens that cause more invasive and aggressive infections. These bacteria enter the body even when no injury to the protective layer is apparent, and they can cause rapidly expanding and contagious diseases.

The Schepens researchers grew epidemic conjunctivitis bacteria (a strain of S pneumoniae) in a culture. They then applied the fluid that the bacteria were cultured in to cell lines that mimicked the eye’s surface, including the presence of intact mucins. They found that the membrane-anchored mucins were cut off and released from the surface of the cells, which allowed the bacteria to enter the cells.

Using mass spectrometry, the researchers then were able to identify an enzyme as the culprit. They confirmed their findings by inactivating the gene in the bacteria that produced this enzyme, and they demonstrated that the bacterium no longer could remove the mucins from the membrane.

“This discovery is a major breakthrough in this long unsolved puzzle about how ‘epidemic’ bacteria enter the body and has given us a new target for drugs that could even be used preventatively,” Dr. Gipson said.

To view the entire study, “A metalloproteinase secreted by

Streptococcus

pneumoniae

removes membrane mucin MUC16 from the epithelial glycocalyx barrier,” go to:

www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0032418

.

For more articles in this issue of Ophthalmology Times eReport, click here.

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