The Nolan Lab studies systemic inflammation related to the host response to sepsis. Innate immune mediators such as the costimulatory mediators CD40/80/86 and their associated ligands are key to sepsis. Work that is more recent has focused on understanding clinical predictors of acute hemodynamic decompensation in sepsis. Finally, using a murine model of sepsis, Dr. Nolan’s group is studying the systemic effects of fluid resuscitation, a mainstay of sepsis treatment.

Related Publications

Lee YI … Nolan A. Fluid resuscitation-associated increased mortality and inflammatory cytokine expression in murine polymicrobial sepsis. J Clin Transl Sci. 2017. DOI.

Lee YI … Nolan A. Predictors of acute hemodynamic decompensation in early sepsis: An observational study. J Clin Med Res. 2016. DOI.

Kobayashi H … Weiden MD. Neutrophils activate alveolar macrophages by producing caspase-6-mediated cleavage of IL-1 receptor-associated kinase-M. J Immunol. 2011. DOI.

Nolan A … Gold JA. Differential role for CD80 and CD86 in the regulation of the innate immune response in murine polymicrobial sepsis. PLoS ONE. 2009. DOI.

Nolan A … Gold JA. CD40 and CD80/86 act synergistically to regulate inflammation and mortality in polymicrobial sepsis. Am J Respir Crit Care Med. 2008. DOI.