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Researchers have created a new method to accelerate wound healing.

Researchers have found a new method to accelerate how wounds heal in humans.  

A team of scientists from Uppsala University and SLU has discovered that lactic acid bacteria can be transformed into human chemokine-producing vectors to bioengineer the wound microenvironment and greatly accelerate wound closure.

The researchers are the first to develop the concept for topical use. The technology could turn out to be disruptive to the field of biologic drugs.

Treating large and chronic wounds is a large and expensive burden on the healthcare system, because there are not many effective tools that accelerate healing. Wound care is limited to mechanical debridement, the use of different dressings and significant amounts of antibiotics to prevent or treat wound infections.

A treatment that kick-starts and accelerates wound healing would have a significant impact due to the aging population, occurrence of chronic diseases including diabetes and the global spread of antibiotic resistances.

Drug candidates currently in late stage clinical trials comprise of growth factors, which are traditional protein-based biological drugs associated with high costs, and some trials have been prematurely terminated.

“We have developed a drug candidate, a next-generation biologic medical product, and are now publishing the fantastic results from the preclinical part where wound healing was strongly accelerated in mice,” Mia Phillipson, a professor at the Department of Medical Cell Biology, Division of Integrative Physiology, Uppsala University, said in a statement.

The newly discovered technique  accelerates the healing process because it leads to changes in the microenvironment in the wound, which changes the behavior of specific immune cells.

The new technology would allow the researchers to increase the level of CXCL12—a chemokine—for a sufficient time period through continuous delivery directly to the wound surface. The bioavailability of CXCL12 is also synergistically increased within the wound as the bacterial produced lactic acid causes a slight pH drop that inhibits degradation.

“The chemokine, CXCL12, is endogenously upregulated in injured tissue and by increasing the levels further, more immune cells are recruited and are more specialized to heal the wound, which accelerates the whole process,” Phillipson said.

The researchers tested the new technology on healthy mice, as well as in mice with two models of diabetes---one model of peripheral ischemia and one model using human skin biopsies.

There were clear differences in the composition of immune cells in the wounds and the immune cells present produced higher levels of TGFß at earlier time points.

“This is very exciting from a health care perspective,” Phillipson said. “We have a technology that works and now understand the mechanism behind it, how it accelerates wound healing.

“The next step is a study in a pig model,” she added.        

 

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