New Technology developed for faster healing of chronic wounds

Published On 2018-02-08 14:30 GMT   |   Update On 2018-02-08 14:30 GMT

Chronic wounds comprise a growing clinical problem that represents >3% of the healthcare budget in industrialized countries. Drug development is hampered by the proteolytic nature of the wounds, which greatly limits drug bioavailability. A new technology that circumvents this by on-site production and reduced chemokine degradation has been developed by Researchers at Uppsala University for faster healing of wounds.Their findings have been published in journal PNAS.The new way of accelerating wound healing involves the use of lactic acid bacteria as vectors to produce and deliver a human chemokine on site in wounds.






Impaired wound closure is a growing medical problem associated with metabolic diseases and aging. Immune cells play important roles in wound healing by following instructions from the microenvironment. The researchers developed a technology to bioengineer the wound microenvironment and enhance healing abilities of the immune cells.Lactobacilli bacteria were transformed into CXCL12-producing vectors to bioengineer the wound microenvironment after topical application. Consequently, the immune cells driving the healing process were reinforced, which greatly accelerated wound closure in healthy mice, in mouse models of hyperglycemia and peripheral ischemia, and in a wound model using human skin disks. Initial safety studies demonstrated that neither bacteria nor the chemokine produced was detected in systemic circulation following application to open wounds.





"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," says Mia Phillipson, professor at the Department of Medical Cell Biology, Division of Integrative Physiology, Uppsala University.


Development of drugs accelerating wound healing is limited by the proteolytic nature of wounds. The new technology overcomes this by on-site chemokine production and reduced degradation, which together ensure prolonged chemokine bioavailability that instructed local immune cells and enhanced wound healing.


"The chemokine, CXCL12, is endogenously upregulated in injured tissue and by increasing the levels further, more immune cells are recruited and are more specialised to heal the wound, which accelerates the whole process," says Professor Phillipson.


For more details click on the link: https://doi.org/10.1073/pnas.1716580115

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