"Sepsis is a life-threatening condition that occurs when the immune system overreacts to an infection. If not immediately treated, sepsis can lead to severe organ damage and even death. According to recent data from the Centers for Disease Control and Prevention, an estimated 1.7 million adults in the U.S. develop sepsis every year and roughly 350,000 will die from the disease. The rapid administration of antibiotics and other supportive care, including IV fluids, can help fight infection, but this approach only scratches the surface."
"The rapid administration of antibiotics and other supportive care, including IV fluids, can help fight infection, but this approach only scratches the surface, according to Hasan Alam, MD, chair and the Loyal and Edith Davis Professor of Surgery who was a co-author of the study. "We give IV fluids and we give antibiotics directed towards the bacteria, but the downstream cascades of what's happening at the cellular level are often not addressed," said Alam, who is also a professor of Cell and Developmental Biology. "Even if we kill the bacteria, we also know that even dead bacteria and bacterial debris is also pro-inflammatory, so that's why antibiotics don't work right away.""
"Sepsis causes immune dysregulation driven by specialized white blood cells called neutrophils. Under normal conditions, neutrophils create neutrophil extracellular traps (NETs) which trap and kill bacteria by releasing citrullinated histone H3 (CitH3), a protein located in the nucleus. In the case of sepsis, the excessive production of NETs can lead to immune dysfunction and tissue damage. In the current study, Alam and his collaborators aimed to target this immune dysfunction by developing a novel anti-CitH3 monoclonal antibody which binds to CitH3 to regulate inflammation."
A novel anti-CitH3 monoclonal antibody binds citrullinated histone H3 to regulate inflammation and reduced immune dysregulation in mouse models of sepsis. Sepsis arises when the immune system overreacts to infection and can cause severe organ damage or death if not treated. Standard care such as rapid antibiotics and IV fluids combats infection but does not immediately resolve inflammatory cascades or effects of bacterial debris. Neutrophils form NETs that release CitH3 to trap pathogens, and excessive NET formation during sepsis drives tissue damage. Targeting CitH3 with a monoclonal antibody offers a strategy to mitigate NET-driven inflammation.
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