Synopsis
A team of scientists from the US has revealed how a specific molecule on certain bacteria may lead to blood clotting in sepsis, a critical condition causing millions of deaths annually. This discovery could significantly improve treatment options for seriously ill patients.Key Takeaways
- Discovery of a molecule related to blood clotting in sepsis.
- Potential for improved treatments for critically ill patients.
- Focus on lipopolysaccharide (LPS) and its role in clotting.
- Identification of factor XII as a therapy target.
- Development of precision therapies based on bacterial strains.
New Delhi, Jan 18 (NationPress) A group of scientists from the United States has discovered how a molecule present on certain bacteria could stimulate blood clotting during sepsis—a severe condition responsible for approximately eight million deaths annually.
The research team at Oregon Health & Science University (OHSU) investigated the specific mechanisms of blood clotting involved in sepsis.
Their results could lead to improved treatments for those in critical condition. They identified that lipopolysaccharide (LPS), a molecule found on the surface of specific bacteria such as E. coli, can directly activate blood proteins that instigate clotting.
This mechanism can obstruct blood flow and harm essential organs through a chain reaction where blood proteins collaborate to form clots. The researchers highlighted a particular type of LPS known as O26:B6, which is notably effective at triggering this clotting response, increasing the risk of clotting complications.
The findings, published in the Journal of Biological Chemistry, stem from a study involving nonhuman primates. The team observed that when bacteria containing LPS entered the bloodstream, it swiftly activated the clotting system.
This activation involved coagulation proteins such as factor XII, which appears to initiate the clotting cascade, leading to a chain reaction. Joseph Shatzel, a physician-scientist at OHSU, noted, “Individuals born without factor XII are healthy and do not experience abnormal bleeding.”
“This makes it an excellent target for therapies—blocking it may help prevent harmful clots without inducing bleeding,” he added.
Andre L. Lira, the lead author and postdoctoral scholar, explained that his research delves into how the physical characteristics of bacterial surfaces trigger the clotting mechanism. Sepsis can result from bacterial, viral, or fungal infections.
“Even when the bacteria responsible for the infection is known, various strains might behave differently,” he stated. “By comprehending this, we aspire to create precision therapies.” The team is currently developing experimental treatments aimed at factor XII, including antibodies designed to inhibit its function.
