A tool the human body possesses to fight off infections in a wound may also actually slow down the healing process, according to new research by a team of scientists from Harvard University in Cambridge, Mass., Boston Children's Hospital, and Penn State University in University Park, Pa.
The researchers found they could accelerate the wound healing process in diabetic mice by preventing immune cells called neutrophils from producing structures called neutrophil extracellular traps, or NETs, that trap and kill bacteria.
NETs reduce the risk of infection in a wound but they also form a dense, toxic mesh that interferes with the mobilization of new healthy cells and hinders tissue repair, especially in those with type 1 and type 2 diabetes.
According to Denisa Wagner, PhD, senior investigator of the Program in Cellular and Molecular Medicine at Boston Children's Hospital and professor at Harvard Medical School, NETs predispose patients to inflammation, heart disease and deep-vein thrombosis — all of which are elevated in patients with diabetes.
"Any injury that causes inflammation will result in the production of NETs, and we think that if the injury involves skin repair, NETs will hinder the repair process," said
The research team treated mice with DNase 1 — an enzyme that breaks up DNA and therefore can destroy NETs. After three days, wounds on DNase 1-treated diabetic animals were 20 percent smaller than on untreated animals.
Interestingly, DNase 1 treatment appeared to accelerate wound healing in healthy mice, as well.
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