Lipopolysaccharide, a virulence factor produced by bacteria, is a toxin that can cause systemic inflammation via the bloodstream. A recent study by scientists at the University of Helsinki identified genetic markers associated with a heightened level of lipopolysaccharides (LPS) in the blood. The results were published in the Journal of the American Heart Association.
The researchers measured LPS levels in the blood of more than 11,000 Finns, after which genome-wide association analyses were carried out to chart the link to the genome. Utilized in further analyses was the FinnGen cohort, which includes genome and disease data on close to 200,000 Finns. The study was carried out collaboratively by the University of Helsinki, the Folkhälsan Research Center, the Finnish Institute for Health and Welfare, and the French Institute of Health and Medical Research.
“As an entirely new find, we identified an apparent link between the human genome and the number of bacterial toxins in the blood,” says researcher Jaakko Leskelä. Blood coagulation and defense against infections are interlinked traits. In the recently published study, a link between endotoxemia and certain genes associated with blood coagulation was found.
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“Our findings connected endotoxemia particularly with blood clots, strokes, and other diseases related to blood coagulation,” Leskelä says. Consequently, the genes which have a favorable effect on wound healing also have an unfavorable connection to low-grade inflammation in the body. “While we do not yet know how exactly these genes associated with coagulation can affect endotoxemia, demonstrating a link is a big step forward as such,” Leskelä notes.
The results also indicate that the quality of the human microbiome makes a difference in the risk of developing cardiovascular diseases. “We have a long road ahead of us in investigating this finding further. However, it is already clear that our results can help to discover new methods for studying and treating low-grade inflammation associated with endotoxemia,” Leskelä concludes.