We are pleased to announce that Dr. Thomas Kehl-Fie, PhD, and Dr. Filiz Korkmaz, PhD, who recently joined the department have transferred their grants to the University of Iowa. 

Dr. Thomas Kehl-Fie, PhD, newly-appointed Associate Professor in Microbiology and Immunology, has transferred his National Institutes of Health/National Institute of Allergy and Infectious Diseases R01 Research Grant titled: “Leveraging host-imposed metal starvation to elucidate the molecular and environmental factors that dictate metal utilization by the iron/manganese superoxide dismutase superfamily”. This grant recognizes that superoxide is a threat to all forms of life and its toxicity is harnessed by the immune system to combat infection. Superoxide dismutases are metal utilizing enzymes that enable us and invading microbes to cope with superoxide, yet we do not know the molecular or environmental factors that dictate the metal utilized by these enzymes. The proposed studies will address this unanswered question, providing insight into how both humans and invading pathogens overcome the universal threat of superoxide. This project involves collaboration with Dr. Kevin Waldron, Associate Professor at the Institute of Biochemistry and Biophysics in Warsaw, Poland.

Dr. Filiz Korkmaz, PhD, newly-appointed Assistant Professor in Microbiology and Immunology, has been awarded a National Institutes of Health/National Heart Lung and Blood Institute 3-year R00 Research Grant titled: “Establishing Mechanisms of LOX-1 Dependent Immune Regulation During Pneumonia”.  This grant recognizes that pneumonia is the leading cause of infection-related deaths worldwide, necessitating a greater understanding of the mechanisms that regulate immune defense and tissue recovery in the lung. Lectin-like oxidized low-density receptor-1 (LOX-1) is a C-type lectin scavenger receptor that has a unique function in the lung, whereby it is protective against edematous lung injury and inflammation through alterations in leukocyte response that results in a pro-resolving phenotype. How LOX-1 promotes the resolution of infection in the lung via resident and recruited leukocytes is not known and is the subject of the proposed studies, where the effects of LOX-1 signaling will be investigated at the level of immunometabolism; and, the consequences of metabolic changes on immune cell activity will be further investigated in the context of lung infection, shedding light on the role of metabolic dysfunction on susceptibility to pneumonia.