Abstract
Sepsis, a life‐threatening clinical condition affecting more than 1.5 million Americans per year, is defined as an over‐exuberant immune response to infection. Currently, sepsis is the leading cause of death in U.S. hospitals, and the incidence of sepsis caused by Gram‐negative bacteria, such as Escherichia coli (E. coli), has been steadily increasing since the late 1990's. While the detailed mechanism of sepsis is not fully understood, several bacterial components are thought to contribute to the hyper‐inflammatory response in humans. Past studies suggest that one E. coli lipoprotein, Peptidoglycan‐Associated Lipoprotein (Pal), may contribute to inflammation and the pathogenesis of sepsis. This work describes our efforts to elucidate the role of Pal in E. coli sepsis and the effect of antibiotics in Pal release from E. coli using a mouse model of sepsis. Our preliminary results corroborate the hypothesis that Pal releases from E. coli and contributes to inflammation and sepsis.Support or Funding InformationRochester Institute of TechnologyThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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