Key Points
Scientists identify LPS molecule driving dangerous blood clotting
Specific bacterial surface triggers can activate clotting proteins
Research may lead to targeted sepsis treatment strategies
The team at Oregon Health & Science University (OHSU) focused on the role of specific blood clotting mechanisms in sepsis.
The findings may pave the way for enhancing treatments for critically ill patients. They found that lipopolysaccharide, or LPS -- a molecule found on the surface of certain bacteria like E. coli -- can directly activate proteins in the blood that trigger clotting.
This process can both block blood flow and damage vital organs in a chain reaction where proteins in the blood work together to form clots. The researchers found a specific type of LPS, called O26:B6, that is particularly good at setting off this reaction, making it more likely to cause clotting problems.
The research, published in the Journal of Biological Chemistry, is based on a study conducted in nonhuman primates. The team found that when bacteria containing LPS entered the bloodstream, it quickly activated the clotting system.
This included coagulating proteins like factor XII, which seems to initiate the clotting process, causing a chain reaction. "People who are born without factor XII are healthy and don't bleed abnormally," said Joseph Shatzel, a physician-scientist at OHSU.
"That makes it a great target for therapies -- blocking it might help stop dangerous clots without causing bleeding."
Andre L. Lira, Postdoctoral scholar and lead author of the study, said his research focuses on how the physical properties of bacterial surfaces trigger the clotting system. Sepsis can arise from bacterial, viral, or fungal infections.
"Even when we know the bacteria causing the infection, different strains can behave differently," he said. "By understanding this, we hope to develop precision therapies." The team is working on experimental treatments targeting factor XII, including antibodies designed to block its activity.
