Delhi Delhi. A team of US scientists has discovered how a molecule found on certain bacteria can promote blood clotting in sepsis – a life-threatening condition that causes the deaths of about eight million people each year.Oregon Health & The team from the University of Science (OHSU) focused on the role of specific blood clotting mechanisms in sepsis.

The findings could pave the way to improving treatments for critically ill patients. They found that lipopolysaccharide, or LPS – a molecule found on the surface of some bacteria like E. coli – can directly activate proteins in the blood that trigger clotting. This process can block blood flow and damage vital organs in a chain reaction where proteins in the blood work together to form clots. Researchers found a specific type of LPS, called O26:B6, that is particularly good at triggering this response, making it more likely to cause clotting problems.

The research, published in the Journal of Biological Chemistry, is based on a study conducted in non-human primates. The team found that when LPS-containing bacteria enter the bloodstream, it quickly activates the clotting system. This included coagulation proteins such as Factor XII, which initiate the clot formation process, causing a chain reaction.

“People who are born without Factor XII are healthy and do not bleed abnormally,” said Joseph Schatzel, a physician-scientist at OHSU. “This makes it a great target for therapies – blocking it could help prevent dangerous clots without bleeding.” Postdoctoral scholar and lead author of the study, Andre L. Lira said her research focuses on how the physical properties of bacterial surfaces activate the clotting mechanism. Sepsis can result from bacterial, viral, or fungal infection. “Even when we know which bacteria causes an infection, different strains may behave differently,” he said. “By understanding this, we hope to develop precise treatments.” The team is working on experimental treatments targeting Factor XII, including antibodies designed to block its activity.