Your skin is coated with acid. While that might sound disturbing, the mild acidity of the skin's surface actually helps to maintain the strength and cohesiveness of the skin. Now researchers at the San Francisco Veterans Affairs Medical Center have discovered where this acidity comes from, and they suggest how it may help to hold the skin together.
The findings, published in the latest issue of the Journal of Investigative Dermatology, may be used to develop therapies for skin problems such as psoriasis.
For decades scientists have known that the outer layers of the skin are about as acidic as a bowl of crushed tomatoes. This acidity was believed to help ward off infections by preventing the growth of bacteria. But the source of all this acid and how it helped to maintain the skin's strength and integrity, remained a mystery.
In their latest study, Joachim Fluhr, MD, a postdoctoral research fellow at the SFVAMC and UCSF, and his colleagues lead by SFVAMC dermatologist Peter Elias, MD, a UCSF professor of dermatology, tested the hypothesis that the acid is produced when enzymes break down fat-like molecules in skin cells, called phospholipids, into smaller acid-tipped fat molecules called fatty acids.
To test this theory, the researchers used a hairless breed of mice and treated patches of their skin with a chemical that blocks the conversion of phospholipids to fatty acids. They then observed what effect this treatment had on the skin.
The treated skin quickly lost its acidity, and this change also had a negative effect on the skin's integrity, Fluhr said. Treated patches of skin were more susceptible to evaporation and drying than untreated skin, he said.
Furthermore, the reduced acidity also made the skin less cohesive. When the researchers repeatedly applied strips of adhesive tape to the skin, they found that significantly more protein stuck to the tape from the inhibitor treated skin than from normal skin.
"We have shown clearly that the skin is generating the acid as it converts phospholipids into fatty acids, one of the natural steps in the formation of the skin barrier. Blocking this conversion has a marked effect on the acidity as well as the skin's integrity and cohesiveness," Fluhr said.
Other experiments suggested a possible explanation for how acidity might help to preserve the skin's integrity. By examining skin samples under a confocal microscope, they found that skin treated with inhibitor drugs had fewer desmosomes, which act like staples to fasten skin cells to one another.
"The protease enzymes that break apart these desmosomes are sensitive to the pH, or acidity, of the skin. So it makes sense that when the pH becomes more acidic, these enzymes are activated to break apart the desmosomes, allowing skin cells to be shed more easily," said Elias.
The findings in the study could aid the development of drugs to treat diseases in which the skin's acid production is out of balance. One example might be psoriasis, in which skin cells are too cohesive and pile up on the skin's surface, Fluhr said. "It may be that by artificially adjusting the skin's surface acidity, we can optimize its barrier function and promote improvements in skin health," he said.
Co-authors on this study included: Jack Kao, SFVAMC dermatology researcher; Sung Ahn, MD; Kenneth Feingold, MD, SFVAMC physician and UCSF professor of medicine; and Mahendra Jain, professor of chemistry and biochemistry, University of Delaware.
The San Francisco Veterans Affairs Medical Center has been a primary affiliate of University of California, San Francisco since 1974. The UCSF School of Medicine and the SFVAMC collaborate to provide education and training programs for medical students and residents at SFVAMC. SFVAMC maintains full responsibility for patient care and facility management of the medical center. Physicians at SFVAMC are employed by the Department of Veterans Affairs and also hold UCSF faculty appointments.
The above post is reprinted from materials provided by University Of California - San Francisco. Note: Materials may be edited for content and length.
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