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Laura Whitmore

Mentor: Jessica Moreland, M.D.
Lab Room: 1283 CBRB
Lab Phone: 319-335-4319

Investigating the role of NADPH oxidase 2 (Nox2) in the resolution of systemic inflammatory responses

Systemic inflammatory response syndrome (SIRS) is a serious condition present in >50% of intensive care unit patients. As patients with SIRS may experience excessive inflammation leading to mortality, the basic mechanisms underlying the resolution of SIRS require intense investigation. Following an inflammatory stimulus, neutrophils and monocytes rapidly migrate toward the site of inflammation where they release molecular mediators including reactive oxygen species (ROS) generated by the NADPH oxidase 2 (Nox2) enzyme complex. It is well established that Nox2-dervied ROS are necessary for eliminating certain pathogens and that excessive ROS can cause host tissue injury. However, recent studies suggest that Nox2-derived ROS may also have an anti-inflammatory function. The goal of our research is to improve the understanding of the role of Nox2 in restoring immunological homeostasis following a systemic inflammatory response. Our overall hypothesis is that Nox2-derived ROS are required for the normal resolution of systemic inflammation. In order to probe the mechanism by which Nox2 promotes the resolution of inflammation, we plan 1) to determine the stage(s) of inflammation dysregulated in the absence of Nox2, 2) to establish the cellular source of Nox2-dervied ROS required to resolve generalized inflammation, and 3) to define the oxidant-sensitive elements of inflammatory signaling in neutrophils.

Honors and Awards

  • Pediatric Research Day Poster Award 2012