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By Kathryn Sloniowski
The study was published on September 12 in the journal Cell Host & Microbe. “Trying to catch bacteria in blood could be like catching fish with your bare hands,” says one of the study’s authors, Paul Kubes, PhD, who is a member of the University of Calgary’s Snyder Institute for Chronic Diseases. “Until now, it’s been thought that there was one cell − the macrophage − that was thought to be important in catching bacteria, but we’ve discovered that there’s actually a second cell that comes in and increases your capacity to catch bacteria out of the main stream of blood about five-fold.” The study, which was conducted in animal models, found that “In the process of desperately trying to get rid of bacteria, we’re basically sacrificing ourselves a little,” says Kubes. “So it’s not a surprise that 30 per cent of people affected by sepsis will die.” Based on this research, Kubes says that he and his team, in collaboration with the Centre for Drug and Research Development in Vancouver, are now in the process of screening thousands of different compounds to see if they can come up with a drug that could act as an inhibitor and/or activator of this process. The hope is to eventually find a drug that will allow them to ‘tweak’ the net release process as is needed to effectively fight off sepsis with minimal harm to the body. Sepsis is an inflammatory response generally triggered by an infection. The disease, which affects approximately 750,000 North Americans annually, can affect any part of the body. Common symptoms include a high fever, shallow, rapid breathing, confusion, disorientation and some will develop a skin rash and joint pain. Severe cases cause organ failure and death. This research was supported by Alberta Innovates−Health Solutions, and the Canadian Institutes of Health Research. |
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