Section of Pulmonary / Critical Care
Instructor of Medicine
|BS||2005||Kent State University||Biology with Molecular and Cellular Concentration
|PhD||2011||University of New Mexico Health Sciences Center||Biomedical Science
|Post Doctoral Scholar||2016||University of Chicago||Asthma, allergies and lung injury
The type 2 immune response is widely implicated in the development of asthma and allergic diseases. It is associated with the cytokines IL-4, IL-5, and IL-13, and cells including eosinophils, type 2 innate lymphoid cells (ILC2s), and T cells. While this immune response is generally considered detrimental, it can also be critically important for repairing damaged tissue under certain conditions. Dr. Hrusch is interested in the role of type 2 immunity in the lung in the context of allergy, fibrosis, and acute injury.
Dr. Hrusch's current research focus is acute respiratory distress syndrome (ARDS), which is a result of severe lung injury caused by infection, sepsis, mechanical ventilation, or trauma. ARDS leads to lung edema and a lack of oxygen resulting in a 30% mortality rate. Importantly, no specific therapy exists for patients with ARDS, and currently, supportive care is the only treatment. Therefore, there is an essential need for improved prevention and treatment of this disease. She is studying how the type 2 immune response can be activated in order to repair the damaged lung tissue associated with ARDS.
Using a number of mouse models, she has found that lung injury normally results in activation of innate type 2 immunity, and that mice with defective type 2 responses do not recover from lung injury. She is further examining what cell types are required for protection, and what specific factors are produced by these cells to reduce the effects of lung injury or promote tissue repair. These studies will have important implications for the treatment of ARDS and other lung diseases, as promoting specific type 2 pathways could serve as a prophylactic therapy against injury.
- Stein, M.M.*, C. L. Hrusch*, Gozdz, J.*, Igartua, C., Pivniouk, V., Murray, S., Addison, K., Marques dos Santos, M., Anderson, R.L., Metwali, N., Neilson, J.W., Maier, R.M., Gilbert, J.A., Holbreich, M., Thorne, P.S., Martinez, F.D., von Mutius, E., Vercelli, D., Ober, C., Sperling, A.I. 2016. Innate immunity and Asthma Risks in Amish and Hutterite Farm Children. NEJM. 375(5):411-21. *denotes equal author contribution.
- Kariuki SN, Maranville JC, Baxter SS, Jeong C, Nakagome S, C.L Hrusch, Witonsky DB, Sperling AI, Di Rienzo A. 2016. Mapping Variation in Cellular and Transcriptional Response to 1,25-Dihydroxyvitamin D3 in Peripheral Blood Mononuclear Cells. PloS One, 11(7):e0159779.
- C.L. Hrusch, Tjota M.Y., Sperling A.I. 2015. The role of dendritic cells and monocytes in the maintenance and loss of respiratory tolerance. Curr Allergy Asthma Rep, 15(1):494. PMC4737703
- Tjota M.Y., C.L. Hrusch, Blaine K.M., Williams J.W., Barrett N.A., Sperling A.I. 2014. Signaling through FcR?-associated receptors on dendritic cells drives IL-33-dependent TH2-type responses. J Allergy Clin Immunol, 134(3):706-713. PMC4149927
- Williams, J.W., M.Y. Tjota, B.S. Clay, B.V. Lugt, H.S. Bandukwala, C.L. Hrusch, D.C. Decker, K.M. Blaine, B.R. Fixsen, H. Singh, R. Sciammas, A.I. Sperling. 2013. Transcription factor IRF4 drives dendritic cells to promote Th2 differentiation. Nature Communications, 4:2990. PMC4003872