Ford Lab

Death caused by sepsis is increasing in the U.S. and globally. We are examining changes at the blood/blood vessel interface that is altered during sepsis, leading to multi-organ failure.

The Ford lab has discovered molecules derived from activated leukocytes, including chlorinated lipids and reactive aldehyde-containing compounds. These novel molecules are being investigated as mediators of dysfunction at the blood/blood vessel interface. In particular, these molecules have important roles in activating endothelial cells and altering leukocyte function.

In addition to the mechanistic roles of the lipids, we are also determining their potential as prognostic indicators of human sepsis outcomes. For these research programs, we employe a multidisciplinary, collaborative approach, including bio-organic (chemical synthesis and mass spectrometry) techniques, biochemical methods, physiological models, and translational/clinical validation.

Current and future studies are being directed to discovering molecules related to the leukocyte-produced lipids originally revealed by our lab as well as their potential pathophysiological roles. While these studies are based on the activation mechanisms of neutrophils, we are also mining deeper into the human metabolome and lipidome involved in sepsis using untargeted lipidomics and metabolomics approaches.