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An international collaboration led by scientists at the UT Southwestern Medical Center has identified a new potential therapeutic target against sepsis, a life-threatening disease that can spread quickly through organs damaging the body.
Researchers and collaborators at UT Southwestern in China, France, and Sweden, as well as New York and Pennsylvania in the United States, have made a key discovery regarding the cellular processes that block the pathways in immune cells leading to a sepsis. At a fundamental level, sepsis is an uncontrollable inflammatory response that damages the organs and essential cellular functions causing tissue damage.
"If it is not recognized early and managed quickly, sepsis can lead to septic shock, multiple organ failure and even death," said Dr. Rui Kang, badociate author of this study, badociate professor of surgery at UT Southwestern, which studies sepsis. "Our study provides new insights into sepsis-related immune regulation and is irrefutable proof that immunometabolism is a potential therapeutic target in sepsis."
Immunometabolism is the interaction of the body's natural or innate immune response – how cells detect and respond to threats – and metabolism – how cells convert food into energy and build the blocks that the body needs to function. Immunometabolism is a new field of study combining the two traditionally independent disciplines.
Sepsis occurs when an initial infection spreads through the blood to other parts of the body. Early detection and treatment of sepsis is essential, but it can be difficult to detect and stop before organs and tissues are damaged. Treatments may include antibiotics, fluids, oxygen, dialysis to ensure blood flow to affected organs, and surgery to remove damaged tissue.
"There are problems with the diagnosis and treatment of sepsis that explain why it is so important to find new therapeutic targets that can block the inflammatory response," said Dr. Kang.
In this study in mice, researchers targeted lipopolysaccharide (LPS), a molecule that is part of the outer membrane of Gram-negative bacteria, one of the major pathogens responsible for sepsis and septic shock.
The researchers discovered a pathway involving LPS that could suppress the sepsis response once activated, thus providing a potentially valuable therapeutic target. The study demonstrates that a neurotransmitter (L-adrenaline) can act on a receptor (ADRA2B) to suppress pathway activation (cytosolic LPS-caspase-11) and lethal inflammation higher.
Reference:
Chen, R., Zeng, L., Zhu, S., Liu, J., Zeh, H.J., Kroemer, G., … Kang, R. (2019). The metabolism of cAMP controls the activation of the caspase-11 inflammasome and pyroptosis during sepsis. Progress of science, 5 (5), eaav5562. https://doi.org/10.1126/sciadv.aav5562
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