J Clin Invest: Identify key molecules involved in acute respiratory distress syndrome!

, July 5, 2020 /PRNewswire-BIOON,BioValley,000 (UPI) -- Researchers at the University of Illinois at Chicago (UIC) have found that interleukin 1 beta-- a protein known to activate an immune response-- can destroy signaling proteins that cause acute respiratory distress syndrome (ARDS)The study was published in the Journal of Clinical Research"20-40% of sepsis patients will have ARDS," said communications author Asrar Malik, a distinguished professor of the UIC Schweppe family and director of theof Pharmacology andRegenerative Medicine at the Medical Schoolsepsis is the body's response to severebacteriainfectionsPhoto Source: Malik, et al.
" In acute respiratory distress syndrome, blood vessels leak and fluid builds up in the lungsThis liquid reduces oxygen content and, in severe cases, can lead to multiple organ failureMalik saidAs a result, many people with acute respiratory distress syndrome need to use a ventilator to increase oxygenationA recent example that led to severe ARDS is COVID-19"
although researchers have known for some time that overactive immune responses causeARDS, the exact molecular mechanism is still unclear using the ARDS animal model, Malik and his colleagues found that interleukin 1 beta blocked a protein called cAMP reaction element binding protein (CREB), preventing it from starting a gene that prevents vascular damage The researchers followed the symptoms of acute respiratory distress syndrome in mice and found that these symptoms were reversed by using CREB DNA to increase CREB levels or activate CREB through the drug Cliplan "This study is important because we have found new molecules associated with ARDS," said co-author Dr Jalees Rehman, a professor of regenerative
medicine at the University of Michigan in medicine, pharmacology and "There is a very delicate balance between reducing inflammation and maintaining immune function Overactivation of immune cells in acute respiratory distress syndrome can cause inflammation and injury However, any ARDS treatment needs to avoid undermining the immune system's ability to fight the virus or bacteria that initially cause infection By targeting individual molecules like CREB, we hope to reduce inflammation and lung damage in ARDS while still allowing the immune system to fight off pathogens in an immune response "
has learned from the ARDS study, Malik hopes to further investigate whether targeting CREB also helps reduce visible lung damage in COVID-19." (BioValleyBioon.com) References: Study says key se man in the acute acute distress syndrome Shiqin Xiong et al.
IL-1 beta suppression of VE-cadherin yn dillis-rhydd yn rhyllsydd yn , journal of clinical police (2020) DOI: 10.1172/JCI136908