Ghent, July 29, 2025 – Scientists in Ghent have achieved a major breakthrough in sepsis research. In a study on mice, the researchers demonstrate that vitamin B1 (thiamine pyrophosphate, TPP) restores mitochondrial energy metabolism, drastically reduces lactate production, and increases survival rates in sepsis. The study results were published in Cell Reports.

Sepsis – commonly known as blood poisoning – is the body’s runaway reaction to an infection. Instead of only attacking the pathogen, the immune system goes into overdrive and also attacks the body itself. This affects vital organs such as the heart, lungs, liver, and kidneys, while patients experience an excessive buildup of lactic acid in the blood.

Each year, sepsis affects 49.5 million people worldwide and claims 11 million lives. To date, there is still no targeted treatment for this condition. New research from the VIB-UGent Center for Inflammation Research may now represent a breakthrough. In a study led by Professor Claude Libert, a Ghent-based research team has discovered a simple yet powerful therapeutic approach: a combination of vitamin B1 and glucose.

Vitamin Deficiency Causes an Energetic Blackout
​In 2021, the same research group had already shown that lactic acid accumulates in the blood of sepsis patients because the body can no longer efficiently clear it. Lactic acid is a metabolite that builds up in our muscles after intense physical exercise. Under normal circumstances, lactic acid is processed by the liver, but in sepsis patients, this process comes to a halt. When too much lactic acid remains in the bloodstream, the patient’s blood pressure plummets rapidly, often with fatal consequences.

With a new study, the research group has now uncovered why lactic acid is produced in such large quantities in the first place and how this can be counteracted. The answer turns out to be remarkably simple and clinically relevant: an acute shortage of vitamin B1 in the mitochondria—the cell’s energy factories—forces another molecule, pyruvate, to be converted into lactic acid.

“For the first time, we’ve been able to show that the problem in sepsis is not so much a lack of oxygen, but a fundamental biochemical defect caused by vitamin B1 deficiency,” explains Louise Nuyttens, lead author of the study. “This shuts down the entire energy network in the body and creates a vicious cycle of lactic acid production and organ damage.”

An Effective Treatment for Sepsis
​As the next step, the researchers investigated whether they could restore energy metabolism by administering vitamin B1. In mouse models, they observed that such treatment drastically reduced lactic acid production and improved survival rates. But the real breakthrough came when they combined vitamin B1 with glucose.

“Although it seems logical to give severely ill patients extra glucose, this often leads to more lactic acid production, which is undesirable in sepsis patients. Thanks to vitamin B1, however, we were able to reprogram glucose metabolism. Glucose was safely converted into pyruvate and then into energy, rather than into toxic lactic acid,” explains Louise Nuyttens.
“The results are truly spectacular,” says Prof. Claude Libert. “In our severe sepsis animal models, nearly all mice survived with the combination of vitamin B1 and glucose. This is one of the most powerful metabolic interventions we’ve ever seen, acting on very simple mechanisms that make it quickly translatable to intensive care.”

Bad Blood
​Beyond its scientific impact, the societal relevance is also significant. Sepsis recently returned to the spotlight through the Pano documentary “Bad Blood” on Flemish television channel Eén, which featured testimonies from bereaved families highlighting the dire lack of therapies. These new insights may offer a path toward a globally applicable therapy for a condition as deadly as heart attacks or strokes, but far less recognized.

Although the results of this study are promising, it is important to note that further research is needed before this can be implemented in practice. Research in mice is only the first step toward a potential treatment in humans. Therefore, the findings of this study cannot be applied to humans just yet.

The research group now plans further preclinical studies in larger animal models to test whether this therapy also works in patients already in an advanced stage of sepsis.

Publication

Nuyttens et al. “Unraveling mitochondrial pyruvate dysfunction to mitigate hyperlactatemia and lethality in sepsis” Cell Reports, 2025.

Financing

The research team at the VIB-UGent Center for Inflammation Research was financially supported by FWO, EOS, GOA, the Methusalem Fund, and iBOF.