Manhasset, NY–(business wire)– Sepsis often causes shock and multiple organ failure and is one of the leading causes of in-hospital mortality worldwide. Much of the mystery surrounding sepsis remains, a scientist at the Feinstein Institutes for Medical Research published in his Cellular & Molecular Immunology. The discovery of proteins that inhibit the body’s ability to eliminate bacteria has opened new avenues of therapeutic research.
A new study explores how extracellular cold-inducible RNA-binding protein (eCIRP), an alarm molecule released during sepsis, triggers immune dysfunction. Specifically, eCIRP destroys cells within the immune system. Cells engulf bacteria and secrete both proinflammatory and antimicrobial mediators known as macrophages. Macrophages play an important role in clearing the body of invading bacteria and damaged or dead cells. However, new research shows how eCIRP dysregulates its normal function and contributes to the progression of sepsis.
Led by Ping Wang, MD of the Feinstein Institutes, this study shows how eCIRP disrupts the cytoskeleton (structures that maintain cell shape) in laboratory mice, ultimately leading to impaired macrophage bacterial digestion during sepsis. explains what Conversely, mice treated with eCIRP-deficient or eCIRP-neutralizing antibodies restored macrophage function and reduced bacterial load. Indeed, mice lacking the eCIRP protein showed better survival outcomes.
Dr. Wang, Professor and Chief Scientific Officer at The Feinstein Institute, said: “By reducing the eCIRP molecule, we can reduce bacteria and improve outcomes in patients with sepsis. This new information opens new avenues for research into effective treatments.”
Sepsis affects at least 1.7 million Americans each year, leads to 270,000 patient deaths, and accounts for 30% of all hospital deaths. Sepsis occurs when the body’s immune system triggers inflammation to fight infection. If uncontrolled, this inflammatory response can damage multiple organ systems and is often fatal. Patients with sepsis often show co-occurrence of pro- and anti-inflammatory pathways. This leads to immunosuppression, inability to eradicate invading bacteria, and ultimately susceptibility to secondary infections. Macrophages eliminate pathogens in the body, but during sepsis the ability of macrophages to phagocytize bacteria is impaired. This leads to bacterial overgrowth that can ultimately cause tissue damage and death.
This study suggests that these findings may provide new treatments for sepsis. Currently, targeting sepsis-induced immunosuppression is one of the most impressive therapeutic directions being investigated. Modifying macrophage function to efficiently clear pathogens could be an important therapeutic strategy to protect patients from sepsis. It could also provide a novel therapeutic avenue for restoring host defenses against pathogens to ameliorate conditions in sepsis and potentially other inflammatory diseases.
“Sepsis affects millions of people each year and we need effective treatments,” said Kevin J. Tracy, M.D., Ph.D., president and CEO of The Feinstein Research Institute. “The findings from Dr. Wang and his lab pave the way for exploring new mechanisms that may one day lead to new treatments.”
The Feinstein Institute continues to lead research into the molecular mechanisms of sepsis to develop therapeutics. Most recently, Dr. Wang and co-director of the study received his $3.8 million from the National Institutes of Health to study sepsis and radiation exposure.
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