Bacterial communication impairs wound healing

This image shows colonies of methicillin-resistant Staphylococcus aureus bacteria. Photo credit: Janice Haney Carr, Jeff Hageman, M.H.S, U.S. Centers for Disease Control and Prevention

Researchers at the University of California San Diego School of Medicine have discovered a previously unrecognized mechanism by which Staphylococcus aureus delays wound healing. In a study, published in The Journal of Clinical Investigation, the researchers found that quorum sensing—a process in which bacteria communicate and coordinate behaviour with one another—is a key driver of delayed healing in wounds infected by S. aureus.

The authors conclude that their findings suggest that by using medications to interfere with quorum sensing, it could be possible to enhance wound healing without relying on antibiotics, reducing the risk of the development of resistance and improving healing outcomes for patients.

By studying both mouse and human models of wound healing, the researchers found infection with S. aureus activated the bacterium’s accessory gene regulator (agr) quorum-sensing system, a molecular “switch” that controls bacterial communication and virulence.

Activating the agr system led to a dramatic suppression of key metabolic genes in keratinocytes.

When the investigators disrupted the agr system in S. aureus, it restored normal wound healing and keratinocyte function, even when the bacteria were present at high levels.

In contrast, exposure to harmless bacteria such as Staphylococcus hominis did not impair healing and even promoted beneficial metabolic activity in skin cells.

In addition to the conclusion that targeting the agr system could be a way to reduce the need for antibiotics and improve healing outcomes for patients, the authors say their findings highlight the importance of the wound microbiome and that therapies which preserve or restore healthy skin bacteria could enhance recovery.

“While further research and clinical trials are needed to translate these insights into specific therapies, the results open the door to innovative approaches for managing wound infections, potentially transforming care for patients with chronic and hard-to-heal wounds,” the authors say, in a press release.

The study was led by Michelle D. Bagood, PhD, a postdoctoral researcher, and Richard L. Gallo, MD, PhD, professor and chair of the Department of Dermatology at the UC San Diego School of Medicine. The work was funded, in part, by grants from the National Institutes of Health. Dr. Gallo is a cofounder, scientific advisor, consultant, and equity holder of MatriSys Bioscience.