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A new study by international team of researchers, led by Monash University's Australian Regenerative Medicine Institute (ARMI) gives insights on the mechanism by which the signal triggering the body's initial inflammatory response to injury shuts down.

The study says that in response to a wound to the body, white blood cells, or leukocytes, travel to the site of the injury in order to protect the tissue from infection and immediately start the repair process.

But then, this inflammation, if continued for too long, could compromise the next stage of healing.

Previous studied have identified how the initial process of sending signals work when leukocytes are called to the wounded part of the body. However, the mechanism with which this signal is turned off, was unknown.

The current study has been able to make a breakthrough in comprehending that aspect, and showed that an enzyme called myeloperoxidase is the key to this process.

For the research, the scientists conducted a study involving zebra fish, where they colored the leukocytes and tissues of the fish, in order to monitor the movement of leukocyte and the concentration of chemical signals.

After observation and study of the transparent fish under a microscope, the researchers could see the regulation of white blood cells in the inflammatory phase of the healing process of an injury.

"White blood cell activity is important for determining the balance between repair, scarring and healing. Understanding what regulates leukocyte activity during inflammation should ultimately allow us to manipulate this system and maximise healing and repair," Professor Lieschke of ARMI said.

"Our research has identified a new pathway to target with anti-inflammatory drugs. There is a significant need for new treatment options as current drugs are not effective in all circumstances," he added according to Medical Xpress.

Lieschke added that the findings of the current study are crucial in for the understanding and treatment for the hereditary disease myeloperoxidase deficiency, which affects leukocyte function in approximately one in every 2000 people.

The study was published in Current Biology.