The bacterium Staphylococcus aureus, cause of the common skin infection bullous impetigo, produces a toxin that attacks a protein highly specific for cell-to-cell binding in the outermost layer of the skin, according to a new study funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). Breakup of this protein, say the researchers, not only brings about the characteristic blistering of the infection, but gives the bacterium "an exquisitely specific mechanism to circumvent the skin's protective barrier and spread further." The University of Pennsylvania's John Stanley, M.D., and his colleagues there and at Japan's Keio University found that the toxin, exfoliative toxin A, causes impetigo's blisters when it breaks up the protein Desmoglein 1 (Dsg1), which is responsible for a specialized type of binding in epidermal skin cells. Only the Dsg1 protein is broken up, say the scientists, and not other closely related proteins. The consequent breakdown in skin cell adhesion gives Staphylococcus a way to proliferate and cause more damage.
The above story is based on materials provided by National Institute Of Arthritis And Musculoskeletal And Skin Diseases. Note: Materials may be edited for content and length.
Cite This Page: