Your skin is your body's barrier against the germs of the outside world. Yet the surface of the skin itself is populated by a host of potentially harmful bacteria. When you scrape your knee or cut your finger, your body's natural defense mechanisms step in to help ensure that the bacteria on your skin won't enter your body and make you sick, says Richard L. Eckert, Ph.D., professor and chair of biochemistry and molecular biology at the University of Maryland School of Medicine. Eckert's research, supported in part by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), focuses on one part of that protective mechanism: the role of a protective protein called S100A7 (psoriasin).

Dr. Eckert's research suggests that S100A7 may have an important role in protecting the body from invasion by E. coli. "E. coli is a bacterium that is present on the skin surface, but some forms can produce infection if they penetrate the skin barrier," says Eckert.

S100A7 is present in low levels in intact skin, but is synthesized at high levels in skin wounds. When skin is wounded, Eckert found, S100A7 is released into the wound, where it floats until it encounters an E. coli bacterium. At that point, the protein appears to stick to the bacterium's surface and, in a way that is not well understood, acts to reduce the bacterium's survival.

"The S100A7 present in the wound may be produced in response to the wound, but may also be produced in response to bacteria in the wound environment," says Dr. Eckert. "We speculate that S100A7 may be 'linked' to the surface of the bacterium and that this might be necessary for bacterial kill."

It is interesting that only a part of the S100A7 protein is required for the antibacterial action to take place. Dr. Eckert and his colleagues demonstrated this by removing parts of the protein and showing that smaller parts can kill bacteria.

Although the researchers don't fully understand the implications of their findings, they say S100A7 is a particularly interesting example of how the body has developed a defense mechanism that protects against invasion by a particular type of bacteria. Their findings not only provide a better understanding of the skin's natural defense mechanisms against bacteria, but may also provide clues about the mechanism of some skin diseases.

"S100A7 may also have a role in other skin disease states," says Eckert. For example, it is present at high levels in the epidermal cells of people with psoriasis, an inflammatory skin disease characterized by recurring reddish patches covered with silvery scales. "It is thought that, in this case, it may have a role in attracting immune cells to the tissue, " he says. "However, it may also act as an antibacterial, as E. coli survive less well in the skin of patients with this condition."

This work was also supported by the National Institute of Diabetes and Digestive and Kidney Diseases.

The mission of the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), a part of the Department of Health and Human Services' National Institutes of Health, is to support research into the causes, treatment, and prevention of arthritis and musculoskeletal and skin diseases; the training of basic and clinical scientists to carry out this research; and the dissemination of information on research progress in these diseases. For more information about NIAMS, call the information clearinghouse at (301) 495-4484 or (877) 22-NIAMS (free call) or visit the NIAMS Web site at http://www.niams.nih.gov.

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Lee, KC, Eckert RL et al. S100A7 (Psoriasin) - Mechanism of Antibacterial Action in Wounds. J Invest Dermatol 2007;127:945-957.

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