Monday, November 30, 2009

Genetically Modified Skin Cells May Help Artificial Skin Fight Infection

Severe skin damage, such as in the case of burn victims, generally means a skin graft will be used during the treatment process of the affected areas. These grafts are either a surgically removed portion of the individuals own skin or artificial skin substitutes. Unfortunately, these bioengineered skin substitutes have a notable limitation: “an increased susceptibility to infection”. However, Researchers may have discovered a means to overcome this limitation.

A study conducted by a team lead by Dorothy Supp, PhD, observed that genetically modifying skin cells to produce an increased amount of the protein HBD4 allows the cell to kill more bacteria than normal. HBD4, or Human Beta Defensin 4, is part of class of proteins called defensins that naturally exist in the body to defend against infection. After isolating the HBD4 gene from tissue samples, Supp transferred the gene into keratinocytes (surface skin cells), giving these modified cells an enhanced immune response.

The reason why cultured skin substitutes are so susceptible to infection is that they are isolated from the body’s circulatory system during the actual grafting period. Therefore, they aren’t exposed to the circulated antibiotic drugs given to the patient or the antibodies of the immune system.

Supp postulates that the use of cultured skin substitutes enhanced with genetically modified skin cells is an effective means of reducing the risk of infection. The use of defensins may provide an alternative to the current method of continually applying antibiotic ointments or wraps to the affected areas of a recovering burn victim and would also aid in skin graft survival.

Though the use of cultured skin substitutes has assisted in the recovery of many burn victims, the compromising variable of infection has been an inhibiting factor of the healing process. The research done by Supp provides an efficient means of not only reducing that problem, but it also reduces the dependence on topical antibiotics and the potential for drug-resistant bacteria.


http://www.sciencedaily.com/releases/2007/01/070108093837.htm

Joshua Mott
VTPP 434-501

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