Jerome Anyalebechi and David Swift receive Shock Society Awards
MAY 2022
Jerome Anyalebechi, MD, has received a Shock Society Diversity Enhancement Award, and David Swift, MD, a Shock Society Travel Award. Both are general surgery residents on research sabbatical under the mentorship of sepsis and shock investigator Craig Coopersmith, MD, and transplant immunology researcher Mandy Ford, PhD.
The awards recognized the quality of Dr. Anyalebechi and Dr. Swift's abstracts, which were conducted under Dr. Coopersmith and Dr. Ford's supervision and review, and will provide up to $1,000 for each so they can attend and participate in the 45th Annual Conference on Shock in Toronto, Canada, June 4-7, 2022. The Shock Society is considered the foremost shock and sepsis basic science organization in the world.
The Diversity Enhancement Award additionally acknowledged Dr. Anyalebechi's leadership in attracting and recruiting deserving trainees from a wide variety of backgrounds by co-chairing the general surgery residency's Diversity Committee and serving on the Department of Surgery's DEI Committee. For Dr. Swift, the Travel Award was a highly competitive honor, as only 40 such awards are distributed each year.
The two primary concentrations of Dr. Coopersmith and Dr. Ford's collaborative lab are investigations of aspects of the immunological host response in sepsis, the area in which Dr. Anyalebechi works, and studies of the connection of chronic alcoholism to increased mortality following sepsis, which is Dr. Swift's focus.
Dr. Anyalebechi's study was concerned with determining the T cell type necessary for improved survival with CD28 agonism in septic, immunologically experienced mice. Evidence implicated an immunosuppressive CD8 T cell whose effector function was mediated by IL-10. The study determined that depletion of this T cell during sepsis led to a significant increase in proinflammatory cytokines and worsened mortality.
Dr. Swift's study expanded further on observations that alcohol-consuming mice have significantly lower levels of CD103, a protein found on the surface of immune cells, by evaluating the effects of using an antibody to block CD103 on the immune response following sepsis in mice not exposed to alcohol. He found that the mice experienced worsened post-sepsis mortality. Additional immunophenotyping showed that the effects of CD103 blockade are dependent on both CD8 and regulatory T cells. Finally, CD103 blockade did not affect survival in mice with chronic alcohol exposure.
The combined results of Dr. Swift's investigation illuminated CD103 as a novel mediator of sepsis mortality, and suggested a putative CD103-dependent mechanism for the increased mortality observed during sepsis in the setting of chronic alcohol exposure.