Stephanie J. Bissel, PhD
Research Assistant Professor of Pathology
Dr. Bissel is a member of the Division of Neuropathology.
200 Lothrop Street
Pittsburgh, PA 15213
Office Telephone: 412-624-5452
Lab Telephone: 412-624-5366
- BS - University of North Dakota, 1994
- PhD - University of Pittsburgh, 2005
Research InterestsMy research concentrates on the involvement of immune responses in the pathogenesis of neurodegenerative diseases and in particular on viral and age-induced nervous system disease. During viral infection, neuronal damage can be mediated by direct infection leading to neuronal death or impairment. Although immune responses can promote clearance or suppression of viral replication, these responses are thought to mediate secondary neuronal damage. Using two models of CNS viral infection, we can examine viral-induced neurodegeneration during acute and chronic infection of the CNS. For chronic viral infection, we have focused on dissecting effects of prolonged immune activation on CNS cells using models of lentiviral encephalitis. Since lentiviruses do not directly infect neurons, neuronal damage is thought to be immune-mediated. We have recently focused on acute CNS viral infections using models of influenza encephalitis - a virus that infects neurons. This model will be used to examine whether acute viral infection of neurons leads to prolonged low-grade inflammation and subsequent neuronal damage.
A second area of interest involves regulation of immune cell activation in the CNS by a molecule called YKL-40. YKL-40 is a chitinase-like protein that belongs to the 18 glycosyl hydrolase family of chitinases but lacks enzymatic activity against chitin. We have found YKL-40 expression to be increased in astrocytes in a number of neuroinflammatory diseases including multiple sclerosis, Alzheimer’s disease and viral encephalitidies. Our goal is to understand the role of YKL-40 in inflammation, CNS injury, and CNS tissue remodeling in these diseases.
Selected PublicationsView Dr. Bissel's publications on PubMed
Bonneh-Barkay D, Zagadailov P, Zou H, Niyonkuru C, Figley M, Starkey A, Wang G, Bissel SJ, Wiley CA, Wagner AK. YKL-40 expression in traumatic brain injury – an initial analysis. J. Neurotrauma. (2010) 27(7):1215-1223.
Giles BM, Bissel SJ, Craigo JK, DeAlmeida DR, Wiley CA, Tumpey TM, Ross TM. Elicitation of anti-1918 influenza immunity early in life prevents morbidity and lower lung infection by 2009 pandemic H1N1 influenza in aged mice. J. Virol. (2012) 86(3):1500-1513.
Giles BM, Bissel SJ, DeAlmeida DR, Wiley CA, Ross TM. Antibody Breadth and Protective Efficacy is Increased By Vaccination with Computationally Optimized Hemagglutinin But Not With Polyvalent Hemagglutinin Based H5N1 VLP Vaccines. Clin. Vaccine Immunol. (2012) 19(2):128-139.
Ross TM, Bhardwaj N, Bissel SJ, Hartman AL, Smith DR. Animal models for Rift Valley fever virus. Virus Res (2012) 163(2):417-423.
Bissel SJ, Giles BM, Wang G, Olevian DC, Ross TM, Wiley CA. Acute Murine H5N1 Influenza A Encephalitis. Brain Pathol (2012) 22(2):150-158.
Giles BM, Crevar C, Carter D, Bissel SJ, Schultz-Cherry S, Khurana S, Golding H, Wiley CA, Ross TM. A Computationally-Optimized Hemagglutinin VLP Vaccine Elicits Broadly-Reactive Antibodies that Protect Non-Human Primates from H5N1 Infection. J Inf Dis (2012) 205(10):1562-1570.
Wiley CA, Ross TM, Carter DM, Bissel SJ. Absence of Fetal Transmission of H1N1 Despite Severe Maternal Infection. Influenza and Other Respiratory Viruses (2012) 6(3):e1.
Bonneh-Barkay D, Bissel SJ, Kofler J, Wang G, Starkey A, Wiley CA. Astrocyte and macrophage regulation of YKL-40 expression and cellular response in neuroinflammation – in vivo versus in vitro studies. Brain Pathol (2012) 22(4):530-546. PMCID: in process.
Bonneh-Barkay D, Wang G, LaFramboise WA, Wiley CA, Bissel SJ. Exacerbation of experimental autoimmune encephalomyelitis in the absence of breast regression protein-39/chitinase 3-like-1. J Neuropathol Exp Neurol (2012) 71(11):948-958.