A potentially life-saving treatment for sepsis has been under our noses for decades in the non-steroidal anti-inflammatory drugs (NSAIDs) most people have in their medicine cabinets, a new University of Colorado Boulder study suggests.
Each year more than 1 million people in the United States contract sepsis, an overwhelming immune response to infection. It kills as many as half of those who contract it, sometimes within days, according to the National Institutes of Health.
“NSAIDS like ibuprofen and aspirin are among the most prevalent pharmaceuticals worldwide, with over 30 billion doses taken annually in the United States alone. But their precise mechanisms of action are not entirely understood,” said Hang Hubert Yin, a biochemistry professor at CU Boulder’s BioFrontiers Institute and lead author of the new paper, published today in Cell Chemical Biology. “We provide the first evidence for a novel mechanism of action for NSAIDS, one we believe could have a direct impact on people’s lives.”
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But Yin’s research found that a subgroup of NSAIDs also act strongly and independently on another family of enzymes, caspases, which reside deep within the cell and have recently been found to play a key role in aggressive immune responses, like sepsis.
“For instance, some chemicals derived from bacteria actually penetrate the cell and trigger the caspase response, prompting the cell to commit suicide. This also is known as apoptosis,” said Yin. “Such activation, in turn, potentially causes inflammation.”